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Cardiovascular 


COLLEGE   OF   OSTEOPATHIC    PHYSICIANS 
AND  SURGEONS  •   LOS  ANGELES,  CALIFORNIA 


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THE  EARLY  DIAGNOSIS  OF  HEART  FAILURE 


PRINTED  BY 

SFOTTISWOODE  AND  CO.    LTD.,  LONDON 

COLCHESTER  AND  ETON 


THE  EARLY  DIAGNOSIS  OF 

HEART   FAILURE 

AND  OTHER  ESSAYS 

ON  THE 

HEART  AND  CIRCULATION 

T:  stagey  WILSON,  M.D.  (Edin.) 

F.R.C.P.  (LoND.),  B.Sc.  (Edin.) 

SENIOR   PHYSICIAN,    GENERAL,   HOSPITAL,    BIRMINGHAM 

LECTURER    ON   MEDICINE   IN    THE   DENTAL   SCHOOL   OF   THE   UNIVERSITY 

OF   BIRMINGHAM 


WITH  ILLUSTRATIONS 


NEW   YORK 

WILLLVM  WOOD  AND  COMPANY 
MDCCCCXV 


\A3C- 


PREFACE 


This  volume  consists  of  separate  essays  dealing  mainly  with 
Heart  Failure. 

Its  aim  throughout  is  to  help  the  practitioner,  when  at  the 
bedside  of  his  patient,  by  suggesting  to  him  new  methods  of 
observation  which  give  fresh  insight  into  the  mode  of  the 
heart's  action  in  health  and  disease. 

The  book  traverses  ground  that  is  more  or  less  new,  since 
it  recognises  types  of  cardiac  failure  which  are  often  ignored 
(in  their  early  stages  at  least),  and  indicates  certain  methods 
of  clinical  diagnosis — some  of  them  simple — w^hich  do  not 
receive  full  description,  and  in  several  instances  are  not  treated 
of  at  all,  in  the  ordinary  text-books  upon  the  heart. 

For  example,  such  conditions  as  '  high  diaphragm  '  and 
*  diminution  in  the  area  of  liver  dullness  '  are  rarely  looked 
for  as  signs  of  diminution  of  the  total  volume  of  blood  in 
circulation  ;  nor  is  this  lessened  volume  of  circulating  blood 
generally  recognised  as  a  sign  of  myocardial  weakness. 

Therefore,  in  advancing  new  theories,  advocating  new 
methods,  and  dealing  with  matters  not  hitherto  regarded  as 
of  proved  clinical  importance,  it  is  incumbent  on  the  author 
to  bring  forward  at  the  same  time  adequate  clinical  evidence 
in  their  favour.  Hence  the  numerous  diagrams  and  details 
of  cases  which  are  introduced. 

Practically  no  reference  is  made  to  the  work  of  other 
observers,  and  for  this  defect  the  writer  would  fain  apologise. 
But,  considering  that  he  has  found  it  difficult  to  compress 
within  reasonable  limits  the  results  of  thirty  years'  clinical 
observations  upon  the  heart,  it  is  evident  that  the  introduction 
and  discussion  of  the  work  of  others  would  have  unduly  in- 
creased the  size  of  the  present  volume. 

-J-     b 


/Vl/O     ^    /V\A) 


vl  PREFACE 

As  the  essays  have  been  written  at  various  times  during 
the  last  twenty  years,  and  deal  with  subjects  closely  related 
to  each  other,  it  is  inevitable  that  there  should  be  a  certain 
amount  of  repetition  ;  no  attempt  has  been  made  to  remedy 
this,  the  writer  preferring  that  each  essay  should  remain 
individually  complete. 

At  the  end  of  the  book  will  be  found  a  series  of  summaries 
of  the  points  raised  in  connection  with  each  of  the  main  subjects, 
and  references  are  given  to  the  pages  dealing  with  the  various 
subjects. 

For  instance,  the  subject  of  the  distensibility  of  the 
heart  wall  is  discussed  in  connection  with  its  value  for  classi- 
fication, in  connection  with  heart  failure  in  adolescence  in 
adult  life  and  in  later  life,  and  also  in  connection  with  its 
relationships  to  heart  failure  with  and  without  dilatation. 

These  various  points  are  brought  together  when  the 
subject  of  'Distensibility'  is  summarised  at  the  end  of  the 
book,  and  references  are  given  to  the  pages  in  the  body  of 
the  work,  where  the  subject  is  discussed  more  fully.  The 
same  is  trae  of  '  Heart  Failure  with  Enlargement,'  '  Heart 
Failure  without  Enlargement,'  '  Compensatory  Diminution 
of  the  Blood  Volume,'  &c. 

Some  of  the  less  important  subjects  are  summarised  in  the 
subject  index  at  the  end  of  the  volume. 

It  is  the  author's  hope  that  this  book  will  not  only  prove 
of  direct  chnical  value,  but  also  that  it  will  stimulate  others 
to  explore  and  develop  new  fields  of  clinical  enterprise  in 
connection  with  the  heart  and  circulation. 

In  conclusion,  the  author  desires  to  acknowledge  his 
indebtedness  to  Dr.  Mary  Sturge  for  many  helpful  sugges- 
tions ;  to  his  resident  physicians,  one  and  all,  for  valuable 
aid  in  collecting  clinical  material  in  his  wards  at  the  Bir- 
mingham General  Hospital ;  and  to  Dr.  Leonard  G.  J.  Mackey 
for  much  kind  assistance  and  many  suggestions  in  revising 
proofs. 

Birmingham: 

November  ith,  1914. 


CONTENTS 


PART   I.— ESSAYS   DEALING   3L\INLY   WITH   THE   EARLY 
DIAGNOSIS  OF  HEART  FAILURE 

Essay  L— EARLY  DIAGNOSIS  OF  HEART  FAILURE. 

PAGE 

Introductory — Classification — Distensibility  of  the  heart  in  ado- 
lescence      ..........  1 

Early  Diagnosis  of  Heabt  Failure  with  Enlargemext  : 

1.  In  DISTENSIBLE  hearts 

Symptoms — Physical  signs — Theory  and  method  of  per- 
cussion— Auscultation  of  the  heart — How  to  detect 
the  first  signs  of  cardiac  failure         .  .  .  .12 

2.  In  hearts  of  moderate  distensibility 

DistensibiUty  of  the  heart  in  adult  life — Symptoms  and 

physical  signs  .  .  .  .  ,  .  .31 

Changes  in  the  left  ventricle  in  heart  failure  with  enlargement       .       46 

Early  Dlvgnosis  of  Heart  Failure  without  Enlargement  : 

Theoretical  considerations  : 

In  distensible  hearts,  i.e.  heart  failure  with  small 

HEART      .........  50 

Symptoms  and  physical  signs  ......       54 

Diminution  in  the  size  of  the  heart  a  sign  of  muscular 

failure  in  valvular  disease      .  .  .  .  .62 

Early  Diagnosis  of  Heart  Failure  in  the  Relatively  Rigid 
Heart  of  Later  Life. 

Introductory — Modifications  in  the  signs  and  symptoms  of  heart 
failure  which  result  from  the  increasing  rigidity  of  the  tissues 
in  later  hfe        .  .  .  .  .  .  ...       70 

DistensibiUty  of  the  heart  in  later  hfe         .....       76 

62 


viii  CONTENTS 

PAGE 

Heart  Failure  in  relatively  Rigid  Hearts  : 

1.  With  enlargement    ........  85 

2.  Without  enlargement  in  moderately  strong  hearts     .          .  86 

3.  Without  enlargement  in  decidedly  weak  hearts         .          .  91 

Illustrative  cases — Heart  failure  without  enlargement  comphcating 
pneumonia — With  and  without  enlargement  in  two  patients  over 
eighty  years  of  age   ........       97 

In  cases  of  valvular  disease  in  later  hfe      .  .  .  .  .110 

Diagnostic  difficulties  associated  with  the  diagnosis  of  heart  failure 
in  later  life  as  regards  :  Dysjmoea — Palpitation — Faintness — 
Anginal  pain       .  .  .         .         .         .         .         .         .112 

Diagnostic  value  of  venous  i)henomena  in  later  hfe     .  .  ,     1-32 

Recognition  of  arterial  resistance  as  a  factor  in  heart  failure — 
Recognition  of  the  degree  of  rigidity  of  the  heart  wall — Evi- 
dences of  rigidity  in  valvular  disease — Difficulties  when  one 
ventricle  is  weak  and  the  other  is  strong         .  .  .  .142 

Essay  II.— ON  THE  VALUE  OF  AN  ABNORMAL  RISE  IN 
THE  LEVEL  OF  THE  DIAPHRAGM  AS  A  GUIDE  TO 
THE  AMOUNT  OF  BLOOD  IN  ACTIVE  CIRCULATION. 

High  diaphragm  due  to  malnutrition  in  enteric  fever — Due  to 
starvation  in  the  treatment  of  gastric  ulcer — After  severe 
hajmorrhage— In  anaemia — In  neurasthenia — High  diajihragm 
in  heart  weakness  .  .  .  .  .  .  .  .163 

Essay  III.— DIMINUTION  IN  THE  AREA  OF  THE  LIVER 
DULLNESS  AS  AN  IMPORTANT  SIGN  OF  MYOCARDIAL 
WEAKNESS  OR  OF  DEFICIENCY  IN  THE  TOTAL 
VOLUME  OF  THE  BLOOD. 

Compensatory  diminution  in  the  blood  volume  in  heart  weakness 
and  its  effect  on  the  hver— Variations  in  the  size  of  the  liver 
dullness  as  detected  by  percussion         .  .  .  .  .185 

Diminution  of  the  liver  dullness  due  to  myocardial  weakness — Due  to 
a  shrinkage  in  the  total  volume  of  the  blood  from  haemorrhage, 
from  anaemia,  from  deficiency  of  essential  constituents  of  the 
blood 195 

Essay  IV.— ON  SOME  DIAGNOSTIC  DIFFICULTIES  ASSOCI- 
ATED WITH  DILATATION  OF  THE  RIGHT  VENTRICLE 

Various  types  of  difficulty — Aneurysm  of  the  transverse  arch  of  the 

aorta  simulating  ujiward  dilatation  of  the  right  ventricle        .     209 


CONTENTS  ix 

TAfJE 

DiflSculties  associated  with  the  recognition  of  the  puhuonaiy  and 
aortic  systoUc  murmurs — Of  the  murmurs  due  to  tricuspid 
regurgitation,  the  true  tricuspid  systolic,  the  superior  vena 
cava  murmur,  and  the  murmur  sometimes  produced  at  the 
venous  valves — Of  the  arterial  compression  murmur         .  .215 

PART  II.— ESSAYS  DEALING  MAINLY  WITH  DILATATION 
OF  THE  HEART  DUE  TO  OVERSTRAIN 

Essay  V.— CONDITION  OF  THE  HEART  IN  THE  AN^mA 
OF   ADOLESCENCE. 

Dilatation  of  the  heart  upwards  and  to  the  left — Statistics — Dilata- 
tion due  to  upward  increase  of  the  right  ventricle — Displace- 
ment of  the  apex  upwards — Dilatation  to  the  right — Failure  of 
the  left  ventricle — Cause  of  upward  dilatation — Pathological 
aspects  of  upward  dilatation  ......     227 

The   Puxmonary  Systolic   Murmur — Its   mode  of  jiroduction   .     254 
Other  auscultatory  phenomena — Right  ventricular  third  sound  and 

mid-diastolic  murmur         .  .  .  .  .  .  .279 

Cases  illustrating  cardiac  dilatation  in  the  anaemia  of  adolescence  .       287 

Essay  VI.— THE  HEART  IN  OVERSTRAIN. 

Cases  of  overstrain  in  adolescence — In  adult  hfe — In  later  life — Case 

of  overstrain  resulting  in  lasting  tachycardia         .         .         .     308 

Essay  VII.— TWO   CLINICAL  LECTURES  ON  DILATATION 

OF  THE  RIGHT  VENT:RICLE,  DELIVERED  1894. 

Tliis  earlv  essay  is  practically  a  siimmary  of  Essay  V.  and  of  parts 

of  Essay  I.  .  . ' 329 

Essay  VIH.— ON  DISPLACEMENT?  OF  THE  HEART. 
By  CHANGES  WITHIN  THE  HEART  ITSELF — Aneurysm — Aortic  regurgi- 
tation a  cause  of  downward  displacement      ....     345 

Upwarb  Displacement  of  the  Apex  in  anajmic  dilatation  of  the 
right  ventricle — Statistics  of  its  frequency — Its  relationshij) 
to  the  age  of  the  patient — To  the  amount  of  upward  dilatation 
— To  the  presence  of  dilatation  of  the  ventricle  to  the  right — • 
To  failure  of  the  left  ventricle — Cause  of  upward  displacement 
of  the  apex  .........     348 

Displacement  by  Extrinsic  Agencies      .....     361 
Downwards  by  abnormal  lowiiess  of  the  diapliragm  in  emphysema, 

&c. — In  chronic  venous  congestion  of  the  lungs         .  .     362 

Displacement  upwards  by  rise  of  diaphragm  .  .  .     368 

Lateral  displacement  of  the  heart  .  .  .  .  .371 

Altered  relationships  of  the  heart  when  displaced  .  .  .     379 


X  CONTENTS 

PART    III.— ESSAYS     DEALING    WITH    VALVULAR    DISEASE, 
ESPECIALLY  IN  RELATION  TO  VENTRICULAR  EXPANSION 

Essay  IX.  PACiii 

The  Nature  of  the  Expansion  Pjiase  of  the  Cardiac  Cvcle 

AND  THE  Phenomena  associated  with  it  .         .         .         .     384 

This  essay  is  mainly  a  summary  of  the  three  following  essays  : 

Essay  X. 
The  diastolic  expansion  movement  of  the  ventricles  as  a  factor 
IN  compensation  for  disease  of  the  mitral  valve 

Cardiographic  and  clinical  evidence  as  to  the  movements  of  the  heart     400 

Essay  XI. 
On  the  theory  of  compensation  in  incompetence  and  stenosis  of 

the  mitral  valve  .........     412 

Essay  XII. 
On  the  diastoUc  cardiac  sound  which  causes  spurious  redupUcation 
of  the  second  sound  at  the  apex  and  is  sometimes  called  the 

THIRD  SOUND  OF  THE  HEART  ......       427 

Essay  XIII. 
On  THE  CONDUCTION  of  the  mitral  systoUc  murmur  down   the 

SPINE  :   its  diagnostic  and  progiiostic  value    ....     442 


PART     IV.  — SUNDRY     ESSAYS     BEARING     UPON      THE 
DIAGNOSIS  OF  HEART  FAILURE 

Essay  XIV.— THE  DIAGNOSTIC  AND  PROGNOSTIC  IM- 
PORTANCE OF  PALLOR  AS  A  SYMPTOM  OF  HEART 
DISEASE  AND  HEART  FAILURE. 

Distinction  between  anaemia  and  pallor — Pallor  in  transient  and 
persistent  heart  weakness — Cases  showing  pallor  as  a  sign  of 
faulty  compensation     ........     448 

Essay  XV.— SOME  LEG  PAINS  OF  CIRCULATORY  ORIGIN 

Leg  Pains  due  to  Dilated  Deep  Veins  of  the  Thigh  : 

Pathology — Symptoms — Referred   iiain — Neurasthenia — Illus- 
trative cases — Treatment     ....  .  .      459 


CONTENTS  xi 

PAGE 

Leo  Pains  due  to  Deficient  Blood  Supply: 

Due  to  feebleness  of  the  general  circulation — A  sign  of  iuy(j- 

cardial  weakness   .......  .     467 

Due  to  local  causes  of  interference  with  the  blood  suj^ply — 
Cramp  —  Intermittent  claudication  —  Due  to  vasomotor 
disturbance         .  .  .  .  .  .  .  .471 

Essay  XVI. 
On  the  value  of  reverberation  in  the  diagnosis  of  the  size  antl 

position  of  the  stomach  .......     480 

Essay  XVII.— A  CASE  OE  ARHYTHMIA  WHICH  THROWS 
NEW  LIGHT  UPON  THE  VENOUS  PULSE  AND  THE 
ACTION  OF  THE  AURICLES. 

Summary     of     the     argument — Interjiretation     of     cardiograms — 
Mechanical  stimulation  of  the  ventricle  a  cause  of  extra  systoles 
— Tonic  activity  of  the  auricles  and  great  veins — Work  done  by 
the  extra  systole — Sudden  distension  of  the  auricle  a  cause  of 
an  auricular  contraction — True  contraction  of  the  veins — Inter- 
pretation of  tracings   ......  .  .     489 

Summary  of  Facts  and  Theories  here  Brought  Forward      .     523 
Physiology  of  the  Auricles  and  Veins  in  the  Light  of  this 

Research 528 

SUMMARIES 

A  SUMMARY  AND  INDEX  OF  ARGUMENTS  AND  FACTS 
BROUGHT  FORWARD  IN  CONNECTION  WITH  THE 
DISTENSIBILITY    OF   THE    HEART    WALL 

Factors  which  determine  the  degree  of  distensibility  of  the  heart 
wall — Variation  in  the  distensibility  of  the  heart  according  to 
the  age  of  the  patient  ........     533 

Distensibility  of  the  heart  in  relation  to  heart  failure  without  enlarge- 
ment ...........     537 

Clinical  estimation  of  the  distensibility  of  the  heart         .  .  .     539 

A  SIBIMARY  AND  INDEX  OF  ARGIBIENTS  AND  FACTS 
BROUGHT  FORWARD  IN  CONNECTION  WITH  HEART 
FAILURE  WITH  ENLARGEMENT 

I.  Theoretical  Considerations  : 

Factors   which   determine   the  amount   and  type    of   cardiac 

dilatation    .         .         .  .  .         .         .         .         .542 


xii  CONTENTS 

PAGE 

Various  types  of  dilatation  of  tlic  heart : 

1.  Adult  type 543 

2.  Adolescent  type         .......     54.3 

3.  Intermediate  types    .......     545 

Overstrain  and  its  relationshij)  to  cardiac  dilatation — Appor- 
tionment of  strain  between  the  two  ventricles — Causes  of 

overstrain         ........      545 

II.  Pathological  Aspects  of  Dilatation  of  the  Right  Ventricle 

IN  Adolescence  and  Early  Adult  Life     ....     546 

III.  Clinical  Aspects  of  Heart  Failure  with  Enlargement. 

1.  In    distensible    hearts,   i.e.   the    adolescent    or    upward 

TYPE  of  dilatation  of  the  right  ventricle 
(Jlinical  features  in  general — Changes  in  pulmonary  second 
sound — Pulmonary    artery    sj'stolic     murmur — Third 
sound,  &c.      ........     547 

2.  In  the  moderately  distensible  heart  of  adult  Life    .  .  .     557 

Physical  signs  in  connection  with  the  right  ventricle,  i.e. 

the  adult  type  of  dilatation    .....     558 
Chnical  features  in  general : 

Phenomena  due  to  tricuspid  regurgitation  .  .     559 

Venous  engorgement — Tricuspid  systolic  murmur — 
Superior  vena  cava  murmiu' — Murmiu'  arising 
at  the  venous  valves  .....     559 

Summary  of  Physical  Signs  in   Connection  with  the  Left 

Ventricle        .  .         .  .  .         .  .         .         .561 

Heart     Failure    with     Enlargement     in     Relationship     to 

Valvular  Disease      ........     562 


A  SUMMARY  AND  IXDEX  OF  ARGUMENTS  AND  FACTS 
BROUGHT  FORWARD  IN  CONNECTION  WITH  HEART 
FAILURE  WITHOUT  ENLARGEMENT 

General  considerations  in  connection  wnth  heart  failure  without 
enlargement — In  the  distensible  heart  of  adolescence — namely, 
heart  failure  with  small  heart — In  the  less  distensible 
heart  of  adult  and  later  life  ......     564 

Clinical  features  of  heart  failure  with  small  heart^ — In  less  distensible 

hearts  ..........     567 

Enlargement  of  a  small  heart  a  sign  of  returning  strength        .  .     570 


CONTENTS  xiii 

A  SIBDIARY  AND  INDEX  OF  ARGUMENTS  AND  FACTS 
BROUGHT  FORWARD  IN  CONNECTION  WITH  EARLY 
DIAGNOSIS  OF  HEART  FAILURE  IN  LATER  LIFE 

Early  Diagnosis  more  Difficult  because  :  page 

I.  Changes  in  the  size  of  the  heart  indicative  of  failure  take 
place  less  readily  owing  to  the  increasing  '  rigidity '  of 
its  tissues      .  .  .  .  •  .  •  •  .571 

II.  Changes  indicative  of  pathological  variations  in  the  volume 
of  blood  in  the  thoracic  viscera  and  in  the  liver  take  place 
less  readily  omng  to  the  increasing  rigidity  of  the  fibrous 
tissues  of  the  body         .  .  .  .  .  .  .571 

III.  There  are  difficulties  in  appraising  the  true  value  of  changes 

in  the  strength  of  the  blood  pressure  owing  to  the  frequency 

of  a  pathological  increase  in  the  arterial  resistance     .  .     572 

IV.  There    are    difficulties    associated    with    the    occurrence    of 

myocardial  weakness  due  to  disease  of  the  coronary  arteries     573 
Y.  There  are  difficulties  due  to  the  fact  that  greater  dependence 
has  to  be  placed  upon  general  symptoms  of  heart  failure, 
and  that  they  are  often  misleading  :    such  are  breathless - 
ness,  palpitation,  faintness.  anginal  pain  .  .  .     575 

Summary  of  evidences  of  heart  failiu-e  in  later  Ufe — )Summaiy 
of  venous  phenomena — of  opposing  and  apparently  contra- 
dictory statements         .......     576 

A  SUMMARY  AND  INDEX  OF  ARGTOIENTS  AND  FACTS 
BROUGHT  FORWARD  IN  CONNECTION  WITH  COM- 
PENSATORY DBIINUTION  OF  THE  BLOOD  VOLL^ilE. 

Compensatory  Diminution  of  the  Total  Volutnie  of  the  Blood 
Owing  to  a  Deficiency  of  One  or  More  of  its  Essential 
Constituents     .........     577 

In  starvation — In  lack  of  water  (cholera,  &c.) — In  haemorrhage — In 

neurasthenia,  &c.  ........     578 

Compensatory  Diminution  of  the  Volume  of  Blood  in  Active 

Circulation  owing  to  Cardiac  Inefficiency       .         .         .     578 

Clinical  signs  given  by  diminution  of  blood  in  the  thoracic  viscera,  i.e. : 

1.  Rise  of  diaphragm  (e-sndenced  by  rise  in  the  gastric  resonance 

and  the  liver  dullness  and  retraction  of  the  supra-clavicular 
hollows) 579 

2.  Diminution  in  the  size  of  the  heart    .....     581 

3.  Diminution  in  the  amount  of  distension  of  the  liver  (shown 

by  decrease  in  its  area  of  absolute  dullness)       .  .  .581 


xiv  CONTENTS 


PAflE 


4.  Emptiness    of    the    auriculo-venous    reservoir    (shown    by 

changes  in  the  pulsation  palpable  in  the  jugular  bulb         ,     583 

5.  Emptiness  of  the  veins     .......     583 

.SUMMARY  AND  INDEX  OF  FACTS  AND  ARGUMENTS 
IN  CONNECTION  WITH  THE  AURICULO-VENOUS 
RESERVOIR. 

Anatomical  Considerations  : 

Constitution  of  reservoir     .......     584 

Physiological  Considerations  : 

Tonic  activity  of  its  walls  (both  auricle  and  veins)  and  mainten- 
ance   of    definite    blood    pressure    within    it — Contractile 
activity  of  the  walls  of  the  auricle  and  the  veins — Tonic 
activity  of    the  walls    of   the   right   ventricle  during  its 
relaxation  phase    ........     584 

Physiological  points  in   connection  with   the   venous   valves,    the 

superior  vena  cava,  the  azygos  vein        .....     587 

Pathological    Changes     in    the    Reservoir    and     Clinical 
Phenomena  Associated  with  Them  : 
Dilatation  of  auricle,  of  veins,  &e.  .  ....     588 

Clinical   Phenomena  showiKo  the  Condition  of  the  Reser- 
voir : 
Pulsation  in  the  jugular  bulb — Signs  of  over-fullness  or  emjitiness 

of  the  blood-vessels  of  the  thoracic  viscera  and  of  the  liver     589 

SUMMARY  AND  INDEX  OF  ARGUMENTS  AND  PACTS 
RELATING  TO  COMPENSATORY  PHENOMENA  IN  CON- 
NECTION WITH   THE  HEART  AND  BLOOD-VESSELS. 

Phenomena  connected  with  the  veins  and  arteries — With  the  heart 

— Compensation  in  mitral  regurgitation — In  mitral  stenosis      .     592 

SUBJECT  INDEX 597 


TIJ>r8TRATI0NS 


yiGS.  TAGES 

1-5.  A  Case  in  which  the  Occurrence  of  Gradual  Cardiac  En- 
largement Indicated  Returning  Strength  after  Myo- 
cardial Weakness      .  .  .  .  .  .  66.  67 

6.     A  Case  where  the  Adolescent  Tv-jie  of  Dilatation  occurred 

in  Late  Adult  Life    .  .   " 84 

7-15.  A  Case  of  Severe  Pneumonia  witli  Myocardial  Weakness, 
and  where  Variations  in  the  Cardiac  Strength  were 
shown  by  Daily  Variations  in  the  Size  of  the  Cardiac 
and  Liver  Dulhiess  and  in  the  Level  of  the  Diaphragm    100. 

101,  103 

16-18.     Small  Heart  in  Myocardial  Weakness        .         .         .      118,119 

19.     Small  Heart  in  Vasomotor  Angina    .  .  .  .  .131 

20-21.     Myocardial  Weakness  mainly  Involving  the  Right  Ventricle     157 

22-24.     Cases  showing  Elevation  of  the  Diaphragm  from  Collapse 

of  the  Left  Lung 166,  167 

Fig.  22  :  Normal  Chest.    Figs.  23,  24  :  Collapse  of  Lung. 

25-30.     Case  of  Gastric  Ulcer,  showing  a  High  Diaphragm  due  to 

Starvation 170,  171 

31-33.  Case  of  Gastric  Ulcer  .showing  a  High  Diaphragm      .  .     174 

34.  High  Diaphragm  the  Result  of  Haemorrhage  (hsematemesis)     174 

35-37.  High  Diaphragm  in  Anaemia    ......     175 

38.  High  Diaphragm  in  Myxoedema        .  .  .  .  .175 

39-40.  High  Diaphragm  in  Pericarditis         .  .  .  .  .182 

41.  High  Diaphragm  in  Myocardial  Weakness .  .  .  .183 

42-52.     Case  Showing  Variations  in  the  Size  of  the  Liver  DuUness, 

from  day  to  day,  due  to  Heart  Weakness    .  .        196-199 

53.     Small  Heart  and  Liver  DuUness  m  Arterio-sclerosis  .         .     202 


xvi  ILLUSTRATIONS 

FiaS.  PAGES 

54-55.     iSmall  Liver  Dullness  due  to  Malnutrition  .  .  .     204 

56-57.     Small  Liver  Dullness  in  Neurasthenia        ....     206 

58.     Diagram   showing  the   Area    of    Audition   of   a   Systohc 

Murmur  Arising  in  the  Superior  Vena  Cava         .  ,     224 

59-61.  Photographs  of  Cardiac  Ventricles  from  Above  after 
Removal  of  the  Aorta,  Pulmonary  Artery,  and  the 
Two  Auricles 248 

Fig.  59  :  Normal  Heart.  Pig.  GO  :  Heart  witli  Sliglitly  Dilated  Right 
Ventricle.  Fig.  61 :  Heart  from  Aortic  and  Mitral  Diseases, 
with  Dilatation  and  Hyi^ertrophy  of  both  Left  and  Right 
Ventricles. 

62-63.     Lateral  View  of  Distended  Hearts 249 

Fig.  62  :  Normal  Heart.  Fig.  63  :  Heart  with  Slight  Dilatation  of  tlie 
Right  Ventricle  Upwards. 

64.  Semi-diagrammatic  View  of  a  Normal  Heart  as  seen  in 
Section  through  the  Pulmonary  Artery  and  Right 
Ventricle "  .  .  .249 

65-66.     Case  showing  Loud  Pulmonary  Murmur  when  Recumbent 

and  no  Murmur  when  Erect      .....     256 

67-72.     Cases  showing  Pulmonary  Murmur  and  LTpward  Dilatation 

of  Right  Ventricle,  both  Moderate      .  .  .  .260 

73-76.     Cases  showing  Loud  Pulmonary  Murmur  with  Considerable 

Dilatation 261 

Figs.  73,  74,  and  76  with  Functional  Jlitral  and  Tricuspid  Murmurs  as 
well. 

77-78.     Cases  showing  an    Inconstant    and    Variable  Puhnonary 

Murmur .268 

79-8L     Cases   showing    Moderate    Upward    Dilatation    of   Right 

Ventricle,  but  no  Pulmonary  Murmur       .  .      270,  271 

82-85.     Cases  showing  Great  Dilatation  of  Right  Ventricle.     Pul- 
monary Murmur  Faint    .....      276,  277 

86-91.     Cases  showing  Tricuspid   and   Pulmonary  Murnnn-s  both 

Present 278 

92-93.     Cases  showing  Considerable  Ventricular  Dilatation,  but  no 

Regurgitant  Murmur         ......     281 

94-98.     Cases  Illustrating  the  Occurrence  of  a  Right  Ventricular 

Third  Sound  and  Mid-diastohc  Murmur       .      283,  285,  286 

99.     Case  of  Anaemia  showing  a  high  Apex  Beat  and  a  Normal 

Diaphragm      ........     288 

100.     A  Case  of  Anpemia  showing  a  High  A^x  Beat  with  a  High 

Diaphragm       ........     289 


ILLUSTRATIONS  xvii 

FIGS.  PAGES 

101-106.     Cases  of  Ancemia  showing  Dilatation  of  the  Right  Ven- 
tricle which  mainly  Involves  the  Conus  Arteriosus    293,  295 

107-108.     Two  Cases  of  Anaemia  showing  Broadening  of  the  Cardiac 

Area 299 

109.     Case  of  Anaemia  showing  no  Increase  in  the  Loudness  of  the 

Pulmonary  Murmur  in  the  Recumbent  Attitude      .     302 

110-111.     Case  shomng  a  Pulmonary  Systolic  Murmur  Louder  in 

the  Erect  than  the  Recumbent  Attitude        .  .     303 

112-113.  A  Case  of  Anaemia  showing  Increased  Loudness  of  the 
Pulmonary  Murmur  due  to  Increased  Cardiac 
Vigour  ........     304 

114-115.  Case  show^ing  Extreme  Dilatation  and  Absence  of  Pul- 
monary Mm-mur  .......     305 

116-119.     Cases  showing    Upward    Dilatation    of    the   Heart   in 

Overstrain 311,  312,  314 

120-122.     Case  illustrating  Dilatation  of  Right  and  Left  Ventricles 

in  Overstrain  in  Adult  Life      .....     317 

123.     Low  Diaphragm  in  Case  of  Overstrained  Heart         .  .     319 

124-125.  Case  showing  Extreme  Dilatation  of  Heart  from  Over- 
strain in  Later  Life        ......     321 

126.  Extreme  Dilatation  of  Heart  in  Pya?mic  Pneumonia       .     323 

127.  Case  of  Overstrain  with   High   Diaphragm   and  Small 

Liver  Dullness      .......     326 

128.  Case   showng   Downward    Displacement   due   to  Intra- 

jjericardial  Aneiu^ysm     ......     34(5 

129.  Case  where    Rapid   Dilatation   of  Heart  with   Upward 

Displacement  occurred  in  Acute  Pneumonia  .     360 

130-132.  Cases  showing  Downward  Displacement  of  the  Heart 
by  the  Lowness  of  the  Diaphragm  resulting  from 
Chronic  Over-distension  of  the  Lungs  and  Thoracic 
Veins  with  Blood '    364,  366,  367 

133.  Case  illustrating  the  Normal  Percu-ssion  of  Heart,  Liver, 

and  Stomach         .......     369 

134.  C!ase  showing  Displacement  Upwards  of  Heart,   Liver, 

and  Stomach        .......     369 

135.  Case  showing  Upward   Displacement  of   the  Heart  by 

High  Diaphragm  .......     370 

136.  Case  showing  Rapid  Lateral  Displacement  of  the  Heart 

by  Collapse  of  the  Left  Lung  ....     372 


xviii  ILLUSTRATIONS 

FIflS.  PAGES 

137.     Case  showing  DisplaccinL'iil  of  Heart  to  the  Left    .  .     376 

138-140.     Case  showing  Displacement  of  the  Heart  to  the  Right 

by  (h-adual  Collapse  of  the  Right  Lung   .  .       377,  378 

141 .     Case  showing  Displacement  of  the  Heart  to  the  Right     ,     382 

142-143.     Cardiographic  Tracings  from  a  Case  of  Mitral  Stenosis 

with  a  well-marked  Third  8omid    .  .  .       432.  433 

Fig.  142  :  Tracing  taken  at  Apex,  whicli  was  in  the  Fiftli  Insterpace, 
li  J  inches  from  the  Sternum,  i'ig.  143  :  Tracing  similar  to  Fig.  1-12, 
but  taken  from  near  tlie  Apex  and  wlien  the  Heart  was  acting 
excitedly. 

144-145.  Cardiograpliic  Tracings  from  a  Case  of  Mitral  Regurgita- 
tion with  a  well-marked  Third  iSound      .  .  .     434 

Fig.  114  :  llocord  of  the  First  and  Second  Sounds  on  a  Cardiogram 
from  near  the  Apex.  (Taken  in  the  Fifth  Interspace,  2  inches 
from  the  Sternum.)  Pig.  145  :  Tracing  taken  from  the  Third 
Loft  Interspace,  1,J  inches  from  the  Sternum. 

146-147.  Cardiographic  Tracings  from  a  Case  of  Mitral  Regurgita- 
tion with  a  well-marked  Third  Sound     .  .  .     437 

Pig.  14G  :  From  the  Sixth  Interspace,  4J  inches  from  the  Sternum. 
Pig.  147  :  From  the  Seventh  Interspace  4  inches  from  the  Sternum 
(i.e.  nearly  1  inch  internal  to  the  Apex  Beat). 

148-152.  Cardiographic  Tracings  from  a  Patient  with  a  very  Loud 
Third  Sound,  a  Faint  First  Somid,  and  a  very  Faint 
PresystoUc  Murmur 438,  439 

Pig.  148  :  Tracing  taken  at  Apex  (in  the  Filth  Interspace,  4  inclies 
from  Sternum).  Fig.  149  :  Tracing  taken  in  the  Fourth  Inter- 
space, 1  inch  from  Sternum.  Fig.  1.50  :  Tracing  taken  in  the  Third 
Interspace,  2J  inches  from  Sternum.  Fig.  151  :  Tracing  taken 
in  the  Epigastriirm.  Fig.  152  :  Record  of  the  First  and  Second 
Sounds  on  the  Cardiogram. 

153-154.  Cardiographic  Tracings  from  a  Case  of  Mitral  Regurgita- 
tion and  Stenosis  with  a  well-marked  Third  Sound    .     440 

Fig.  153  :  Tracing  from  the  Apex,  showing  a  Record  of  the  First 
and  Second  Sounds  on  the  Cardiogram,  and  the  Theoretical 
Position  of  the  Third  Sound  as  verified  by  other  Tracings. 
I'ig.  154 :  Tracing  taken  Internal  to  the  Apex  where  the 
Dimuiution  in  the  Volume  of  the  Ventricle  at  the  end  of  the 
Systole  causes  a  Fall  in  the  Tracing. 

155.     Cardiographic  Tracing  from  a  Case  of  Anajmic  Dilata- 
tion of  the  Heart  with  a  well-marked  Third  Sound        441 

Tracing  from  the  Apex  showing  a  record  of  the  Second  and  Thir.l 
Sounds. 

156-163.     Tracings  illustrating  a   Ca.se  of  Arhythmia  with  Extra 

Systoles  .  .  .  .    '     .  .  .     494-520 

Fig.  15C  :  Tracings  from  the  Apex  and  the  Carotid  ^U-tery,  sliowing  tliat 
*  the  Extra  Systole  causes  no  Pulse  Wave  m  tlie  Artery  and  that 

the  Wave  following  an  Extra  Systole  is  smaller  than  uomial. 
Fig.  157 :  Copy  of  a  Tracing  showing  a  Wave  in  the  Jugular 
Vein  which  results  from  the  Extra  S3'stole.  Fig.  158  :  Copy  of  a 
Tracing  upon  which  the  Time  of  Occurrence  of  the  First  and 
Second  Sound  was  marked  by  an  Electrical  Signal.  Pig.  159  : 
Tracing  Demonstratmg  the  Fact  that  there  is  no  Sign  of  any 
Auricular  Wave  preceding  the  Extra  Systole. 
Figs.  160-163  :  Tracmgs  illustrating  the  Interpretation  of  the  Cardio- 
grams and  the  Venous  Tracings  taken  in  this  (^iso. 


ILLUSTRATIONS  xix 


PLATES 

PLATE 

I.  A  Photograph  of  the  Chest,  showing  the  rapid  return  of  the 
Heart  and  Liver  DuUness  towards  Normal  after  a  diminu- 
tion in  size  due  to  Cardiac  Weakness     .     Facing  p.       64 

IT.  Pliotograph  of  the  Patient  Thos.  S.,  showing  the  actual 
Outhne  of  the  Heart,  Limgs,  and  Stomach  (as  deter- 
minable by  Percussion)  marked  upon  the  Chest,  for 
comparison  with  the  Diagrams  illustrating  the  Case 

Facing  p.  326 

III.  Photograph  of  Thos.  S.,  showing  the  Outline  of  the  Viscera, 

as  marked  on  the  Chest,  as  the  result  of  Percussion, 
antero-Iateral  view     .....     Facing  p.  327 

IV.  Photograph  of  the  Chest,  showing  the  Outline  of  the  Heart 

and  Liver  when  Displaced  Downwards  by  the  Descent 
of  the  Diaphragm  owing  to  Chronic  Over-distension  of 
the  Thoracic  Viscera  with  Blood  .  .      Facing  p.  364 

Y.  Photograph  of  the  Chest,  showing  Downward  Displacement 
of  the  Diaphragm  and  Heart  owing  to  the  Chronic  Over- 
distension of  the  Thoracic  Viscera  with  Blood,  antero- 
lateral view  .....     Folloiving  Plate  IV 

VI.  Radiograph  of  the  Chest,  proving  Downward  Displacement 
of  the  Heart  in  a  Case  of  Chronic  Over-distension  of 
the  Thoracic  Viscera  with  Blood  .         Fcllowing  Plate  V 

VII.     Cardiograms  Demonstrating  the  Enlargement  of  the  Ventricle 

during  its  Expansion  Phase.     (Cases  I  to  III.)    Facing  p.  410 

VIII.     Cardiograms  Demonstrating  the  Enlargement  of  the  Ventricle 
during  its  Expansion  Phase.     (Cases  III.  to  X.) 

Facing  p.  41 1 


TRACINGS  ILLUSTRATING  A  CASE  OF  ARYTHMIA 

WITH  EXTRA  SYSTOLES 

(At  end  of  Volume) 

IX.     Xo.  1. — Tracing  taken  Internal  to  Apex  Beat  compared  with  one 
taken  over  the  Carotid  Artery. 

Xo.  2. — Tracing  taken  at  Apex  on  which  was  recorded  the  Time 
of  Occurrence  of  the  First  and  Second  Heart  Sounds  by 
means  of  an  Electric  Signal. 

Xos.  3  and  4. — Upper  Tracing,  Apex  Cardiogram  ;  Lower  Tracing, 
from  Jugular  Bulb. 


XX  ILLUSTEATIONS 

PLATE 

X.     No.  5. — A    Venlricular    Cardiogram    compared    with    a    Tracing 
taken  simultaneously  over  the  Jugular  Bulb. 

Xa.  Xo.  5a. — Enlarged  Photograph  of  the  Original  Blue-ink  Tracing, 
part  of  which  is  shown  in  Plate  X. 

XI.     Xo.  6. — Tracing  taken  over  the  Apex  compared  with  one  taken 
over  the  Jugular  Bulb. 

Xo.  7. — Tracing  taken  a  little  Internal  to  the  Apex  Beat  compared 
wth  one  taken  over  the  Jugular  Bulb  while  the  Heart  was 
under  the  Influence  of  Digitalis. 

Xo.  8. — Tracing  taken  a  little  Internal  to  the  Apex  Beat  compared 
with  one  taken  over  the  Jugular  Bulb,  while  the  Heart  was 
strongly  under  the  Influence  of  Digitalis. 

XII.     Xo.  9. — Auricular  and  Ventricular  Tracings  compared. 

Xn.  10. — Ventricular  Tracing  with  Record  of  First  and  Second 
Sounds. 


HEART  FAILURE 

PART  I.— ESSAYS  DEALING  MAINLY  WITH  THE 
EARLY  DIAGNOSIS  OF  HEART  FAILURE 

Essay    I.— THE    EARLY    DIAGNOSIS    OF    HEART 
FAILURE 

By  heart  failure  is  meant  the  inabiHty  of  the  heart  properly  to 
discharge  its  function  of  circulating  the  blood. 

There  is  no  need  to  dwell  upon  the  importance  of  the 
early  diagnosis  of  heart  failure,  for  the  immediate  recognition 
of  slight  changes  in  the  heart's  efficiency  may  be  a  matter 
of  vital  importance  when  the  medical  practitioner  is  face  to 
face  with  some  serious  cardiac  complication. 

The  clinical  phenomena  which  indicate  slight  alterations  in 
the  efficacy  of  the  heart's  action  do  not  seem  to  have  received, 
as  yet,  the  recognition  which  their  importance  demands,  and 
therefore  much  of  what  will  be  said  in  the  following  pages 
upon  the  subject  may  not  receive  ready  acceptance.  When 
statements  such  as  these  are  made,  however,  detailed  proof 
will  not  be  given  as  a  rule  at  first,  although  in  subsequent 
essays  debatable  points  will  be  taken  up  and  clinical  proof 
submitted.  Were  any  other  com-se  adopted,  the  argument 
advanced  would  be  obscured  and  overburdened  with  detail. 
For  instance,  in  the  present  essay  a  simple  statement  only 
will  be  given  of  the  chnical  and  pathological  phenomena  which 
characterise  the  various  types  of  heart  failure,  together  with 
the  theoretical  considerations  which  harmonise  the  two  sets  of 
phenomena.  The  full  discussion  of  such  signs  and  symptoms 
as  have  not  yet  received  full  recognition  from  the  medical 


2  HEART  FAILURE 

profession  in  general  will  be  deferred  to  subsequent  essays, 
where  clinical  proofs  can  be  given  of  the  points  raised. 

The  fact  that  the  earlier  phenomena  of  heart  failure  are 
alone  to  be  discussed  greatly  limits  the  scope  of  the  subject 
here  dealt  with ;  for  although  the  causes  and  types  of  cardiac 
failure  are  very  numerous,  there  is  nothing  like  the  same 
diversity  in  the  w^ays  in  which  cardiac  failure  of  any  kind 
commences  to  manifest  itself.  Therefore  in  discussing  the 
early  diagnosis  of  heart  failure,  it  will  not  be  necessary  to  go 
into  the  subject  as  a  whole. 

This  is  due  to  the  fact  that,  in  the  majority  of  the  cases, 
heai-t  failure — whatever  its  pathological  cause — first  reveals 
its  presence  chnically  by  phenomena  due  to  a  failure  of  the 
right  ventricle. 

There  are  two  reasons  for  this  prominence  of  the  phenomena 
of  right-sided  failure  : — 

Firstly,  there  are  anatomical  reasons  :  in  that  the  right 
ventricle  is  more  accessible  to  physical  examination  than  the 
left,  occupying,  as  it  does,  most  of  the  anterior  aspect  of 
the  heart,  which  is  the  portion  least  covered  by  the  lungs. 
The  most  dilatable  part  of  the  left  ventricle,  on  the  other 
hand,  lies  deeply  in  the  thorax,  and  is  so  completely  covered 
by  the  lung  that  dilatation  of  the  left  heart  cannot  be  recog- 
nised by  physical  examination  mitil  it  has  reached  a  very 
considerable  extent. 

Another  anatomical  reason  is  that  the  condition  of  the 
veins  entering  the  right  side  can  be  studied  clinically,  whereas 
those  entering  the  left  auricle  cannot. 

The  second  reason  for  signs  of  cardiac  failure  showing  first 
on  the  right  side  of  the  heart  is  a  physiological  one — ^namely, 
the  well-known  fact  that  when  the  left  ventricle  fails,  the 
failure  at  once  throws  more  work  upon  the  right  side  of 
the  heart :  this  being  due  to  the  fact  that  the  left  auricle  is 
not  furnished  with  a  compensation  reservoir,  as  is  the  case 
with  the  right  auricle,  and  therefore  there  is  no  means  of  storing 
any  temporary  excess  of  blood  which  may  result  from  faulty 
propulsion  on  the  part  of  the  ventricle.  Any  delay,  therefore, 
in  the  passage  of  blood  through  the  left  ventricle  must  tend 
to  the  overfilling  of  the  pulmonary  veins  and  a  rise  in  the 


EARLY  DIAGNOSIS  3 

blood   pressure   in  the    pulmonary   artery,    and    thus   throw 
increased  work  upon  the  right  ventricle. 

Therefore,  although  the  left  ventricle  is  the  stronger  chamber, 
it  has,  owing  to  the  absence  of  any  compensation  reservoir, 
to  fall  back  upon  the  right  ventricle  for  support  in  even  a 
temporary  embarrassment.^ 

Therefore,  since — ^in  the  majority  of  instances — cardiac  failure 
first  manifests  itself  by  phenomena  due  to  failure  of  the  right 
ventricle,  the  early  diagnosis  of  heart  failure  consists  mainly 
in  the  early  recognition  of  an  overacting,  or  a  failing,  right 
ventricle. 

Before  taking  up  in  detail  the  discussion  of  the  early  signs 
of  cardiac  failure,  it  will  be  well  to  indicate  broadly  the  lines 
upon  which  they  will  be  classified  in  the  following  pages. 

In  bringing  under  review  the  various  types  of  heart  failure 
it  must  be  recognised  that  the  type  of  change  which  will  result 
from  faulty  action  of  the  heart  will,  in  any  particular  case, 
depend  largely  upon  the  degree  of  elasticity  which  is  possessed 
by  the  cardiac  tissues.  Where  a  heart  is  very  distensible 
the  symptoms  and  their  interpretation,  as  well  as  their  treat- 
ment, are  not  the  same  as  where  the  cardiac  tissues  are  more 
rigid  and  possess  httle  distensibility. 

This  quality  of  distensibihty  can  therefore  be  used  for 
purposes  of  classification,  in  spite  of  the  fact  that  all  cases  of 
cardiac  failure,  looked  at  from  this  point  of  view,  form  a 
continuous  series  ranging  from  the  very  distensible  heart  of 
youth  and  adolescence,  at  one  end  of  the  series,  up  to  the 
comparatively  rigid  heart  that  is  often  seen  in  advanced 
life,  at  the  other  end. 

Such  a  classification,  while  not  of  service  from  a  scientific 
point  of  view,  because  of  the  impossibility  of  dividing  the  cases 
up  into  well-defined  groups  by  means  of  it,  is  yet  eminently 
serviceable  from  a  clinical  standpoint.  The  selection  of  this 
characteristic  of  the  heart  is  amply  justified  because  the 
clinical  phenomena  observable  in  cases  at  the  two  extreme 
limits  of  the  series  are  very  diverse,  and  the  recognition  of  the 

^  This  sentence  takes  for  granted  the  view  that  the  left  ventricle  is  normally 
complete  in  itself — filling  itself  by  its  own  expansion — and  is  not,  under  ordinary 
circumstances,  dependent  upon  the  right  ventricle  at  3i\\(vide  Essay  IX,  p.  384). 

b2 


4  HEART  FAILURE 

amount  of  distensibility  possessed  by  the  heart  is  so  important 
from  the  standpoint  of  prognosis  and  treatment ;  also  in  most 
cases  of  heart  failure  the  true  meaning  of  the  phenomena 
presented  cannot  be  understood  unless  some  estimate  of  the 
amount  of  distensibility  can  be  made.  Dilatation  of  a 
moderately  rigid  heart  shows  a  far  more  serious  degree  of 
failure  than  dilatation  of  an  easily  distensible  heart. 

Before  going  further,  this  quality  of  distensibility  must  be 
more  fully  discussed. 

When  studying  clinically  and  in  the  post-mortem  room,  the 
various  types  of  change  in  the  size  of  the  heart,  which  charac- 
terise cardiac  failure,  the  fact  is  clearly  brought  out  that 
considerable  diversity  is  observable,  not  only  in  the  general 
distensibility  of  the  organ,  but  also  in  the  way  in  which  it 
changes  in  volume  when  called  upon  to  try  to  overcome  a 
hindrance  to  the  circulation  somewhat  in  excess  of  what 
it  is  easily  able  to  meet.  In  some  cases  there  is  evidence 
that  the  heart  is  very  distensible  and  in  others  that  it  is  not. 
For  instance,  on  comparing  the  heart  as  seen  after  death  with 
its  condition  during  life,  it  is  sometimes  found  that  a  heart 
which  was  greatly  dilated  during  life  appears  after  death 
to  show  hardly  any  signs  of  enlargement ;  while  others  will, 
under  the  same  conditions,  show  on  the  post-mortem  table 
almost  the  same  degree  of  enlargement  that  was  noticeable 
during  life.  Again,  some  patients  will  die  of  heart  failure 
without  cardiac  dilatation  under  circumstances  that  do,  in 
other  cases,  produce  enlargement.  Such  facts  point  to  varia- 
tions in  the  degree  of  distensibility  of  the  heart  in  different 
patients. 

Again,  in  some  cases  there  is  evidence  that  the  thinner 
parts  of  the  muscular  wall  are  the  first  to  give  vfay,  whilst 
in  other  patients  this  is  not  the  case. 

If,  for  instance,  we  study  the  way  in  which  the  heart  dilates 
in  adolescence,  we  find  clear  evidence  that  the  main  factor 
which  determines  the  power  of  resisting  dilatation  appears 
to  be  the  thickness  of  the  muscular  wall.  For  the  readiness 
with  which  any  particular  part  of  the  heart  wall  yields  to  any 
excess  of  distensile  force — such  as  occurs  in  physical  overstrain 
— is  found  to  be  proportional  to  its  muscular  weakness.      The 


EARLY  DIAGNOSIS  5 

first  part  to  yield  is  the  thinnest  part  of  the  right  ventricle — 
namely,  that  part  of  the  anterior  wall  which  is  situated  just 
below  the  pulmonary  valves.  The  next  is  the  basal  portion 
of  the  right  ventricle,  which  is  intermediate  in  strength  between 
the  muscularly  strong  apical  part  and  the  thin  part  above 
mentioned. 

Again,  the  difference  in  muscularity  between  the  two  ven- 
tricles seems  to  render  possible  very  considerable  dilatation  of 
the  right  side  in  overstrain  without  any  signs  that  the  left  ven- 
tricle is  giving  way.  Another  point  in  favour  of  the  heart  in 
adolescence  having  to  rely  mainly  upon  its  muscular  strength 
for  its  power  of  resisting  dilatation  is  that  slight  degrees  of 
muscular  malnutrition  seem  to  play  a  more  important  part 
in  favouring  dilatation  than  is  the  case  in  later  life. 

If  we  now  compare  the  phenomena  observable  in  the  adult 
in  cases  of  overstrain,  we  shall  not  find  the  same  readiness 
of  the  thinner  parts  of  the  heart  wall  to  dilate.  The  ddatation 
of  the  right  ventricle  is  more  uniform,  and  there  is  not  the 
same  disparity  in  the  relative  distensibility  of  the  two  sides 
of  the  heart  that  was  observable  earlier  in  life.  In  the  adult 
a  well-marked  dilatation  of  the  right  side  from  overstrain  is 
usually  accompanied  by  recognisable  signs  of  failm-e  of  the 
left  ventricle  also. 

These  observations  seem  to  show  that  while  the  muscular 
strength  of  the  heart  wall  determines  its  power  of  resisting 
dilatation  in  early  life,  in  later  life  dilatation  is  prevented 
by  some  other  factor.  This  factor  is  the  fibrous  tissue  which 
enters  into  the  structure  of  the  heart  and  pericardium. 

Some  work  done  by  the  late  Dr.  Arthur  Foxwell  clearly 
showed  that  the  fibrous  tissue  of  the  pericardium,  and  especially 
that  of  the  parietal  pericardium,  had  an  important  function 
in  preventing  dilatation  of  the  heart. 

The  recognition  of  this  fact  makes  the  solution  of  our 
problem  an  easy  one,  for,  in  the  rapidly  developing  tissues 
of  adolescence,  the  resisting  power  of  the  fibrous  elements 
is  very  low  as  compared  with  their  strength  later  in  life. 

We  can  therefore  make  the  following  generalisations  : — 

In  youth  and  adolescence  the  heart,  owing  to  the  softness 
and  elasticity   of   the   fibrous   tissues   which   enter   into    its 


6  HEART  FAILURE 

composition,  has  mainly  to  rely  upon  its  muscular  tissues  for 
its  power  of  resisting  dilatation.  In  middle  life,  when  the 
fibrous  tissues  become  firmer  and  less  distensible,  they  take 
a  much  larger  share  in  the  prevention  of  over-distension 
than  they  do  in  earlier  life. 

In  later  life  the  relative  rigidity  and  non-distensibility 
which  sometimes  characterise  the  heart  are  presumably  due  to 
an  extreme  hardening  of  the  fibrous  elements  in  its  composition. 

Enough  has  now  been  said  to  explain  what  is  meant  by 
distensibihty  of  the  heart  as  a  basis  for  classification,  and  the 
further  discussion  of  this  quality  can  be  postponed  until  after 
the  subject  of  Classification  has  been  dealt  with. 

Clinical  Classification  of  Cases  of  Cardiac  Failure 

From  the  point  of  view  of  early  diagnosis,  all  cases  of 
cardiac  failure  must  be  divided  into  two  main  classes  ;  for 
while  the  symptoms  of  early  heart  failure  may  often  be  very 
similar,  a  marked  difference  is  recognisable  in  the  'physical 
signs ;  and  all  cases,  whether  in  distensible  or  in  more  rigid 
hearts,   must    be    divided    into    two    main    classes — namely, 

(1)  heart     failure     with     enlargement     of    the     heart,    and 

(2)  heart  failure  without  enlargement. 

In  the  first  group  the  heart  when  having  to  overcome  a 
resistance  to  the  outflow  of  blood,  which  is  in  excess  of  the 
resisting  power  of  its  walls,  is  able  to  raise  its  intraventricular 
pressure  sufficiently  to  empty  itself ;  but  in  so  doing  causes 
over-stretching  of  its  walls.  ("\Miatever  be  the  theory  as  to 
the  mode  in  which  dilatation  is  produced,  the  ultimate  force 
producing  it  must  be  the  muscular  power  of  the  heart.) 

In  the  first  group,  therefore,  the  heart  when  called  upon  to 
do  work  beyond  the  resisting  power  of  the  weaker  parts  of 
its  walls  is  strong  enough  to  do  so,  and,  consequentl}^  dilatation 
results.  This  group,  where  the  heart  muscle  is  relatively 
strong,  may  be  called  Cardiac  Failure  mith  Enlargement 
of  the  Heart. 

In  the  second  group  are  included  cases  where  the  heart 
muscle  is  too  feeble  to  cope  with  the  resistance  wliich  it  has 
to  face.     It  cannot  raise  the  intraventricular   pressure  to  a 


DISTENSIBILITY  OF  THE  HEART  IN  ADOLESCENCE    7 

point  sufficiently  high  to  produce  dilatation  of  the  heart. 
In  this  group  we  have  to  deal  with  cardiac  failure  without 
enlargement,  and  as  a  well-known  illustration  may  be  cited 
the  case  of  fatty  degeneration,  where  a  patient  can  die  of 
heart  failure  without  showing  any  signs  of  dilatation,  of 
engorgement  of  the  veins,  heart  murmur,  or  other  of  the 
generally  accepted  physical  signs  of  heart  failure. 

For  the  purpose,  therefore,  of  discussing  clinically  the  early 
diagnosis  of  heart  failure,  it  is  proposed  to  subdivide  the 
subject  as  follows  : — 

1.  Heart  failure  with  enlargement,  as  it  occurs  in — 

(a)  The  distensible  heart  of  adolescence ; 

(6)  The  moderately  distensible  heart  of  middle  life ; 

(c)  The  more  rigid  heart  of  advanced  life. 

2.  Heart  failure  without  enlargement,  as  it  occurs  in — 

(a)  The  distensible  heart  of  adolescence  ; 

(&)  The  moderately  distensible  heart  of  middle  life ; 

(c)  The  more  rigid  heart  of  advanced  life. 

DiSTENSIBILITY   OF    THE    HeART    IN    ADOLESCENCE 

Before  taking  up  the  discussion  of  the  first  of  these  groups 
it  will  be  well  to  go  a  httle  more  fully  into  the  quality  of 
distensibility  as  manifested  in  adolescence. 

Amount  of  Distensibility. — In  early  life  the  amount 
of  cardiac  distensibility  is  sometimes  remarkably  great,  and 
the  following  is  the  most  striking  instance  of  it  that  I  have 
met  with. 

The  patient  was  a  young  woman,  sixteen  years  of  age, 
who  was  suffering  from  pyaemic  pneumonia.  The  lung 
disease  was  most  extensive,  and  at  the  post-mortem  the  lungs 
were  found  to  be  full  of  pysemic  abscesses.  When  I  saw  her, 
there  was  an  enormous  amount  of  dilatation  of  the  heart.  The 
cardiac  dullness  and  pulsation  extended  from  a  point  one  inch 
to  the  right  of  the  sternum  to  beyond  the  left  anterior  axillary 
line  and  from  the  first  left  interspace  above  down  to  the  fifth 
interspace  in  the  anterior  axillary  hne.  There  were  the  usual 
murmurs  present.  The  patient  died  two  or  three  days  later. 
On   inquiring   as   to   the    condition   of   the   heart   from   the 


8    DISTENSIBILITY  OF  THE  HEAKT  IN  ADOLESCENCE 

pathologist  who  made  the  post-mortem  examination,  I  was 
surprised  to  hear  that  it  was  of  normal  size.  Fortunately,  I 
was  able  to  examine  the  organ  for  myself  and  found  that  there 
was  no  evident  enlargement.  On  testing  its  walls,  however — 
and  especially  those  of  the  right  ventricle  and  the  auricles — 
they  were  found  to  yield  to  an  amount  of  force  that 
would  not  have  been  sufficient  to  stretch  normal  heart  walls. 
With  such  a  degree  of  distensibility  it  w^as  easy  to  beheve 
that  the  heart  walls  w^ould  readily  yield  to  a  raised  blood 
pressure,  and  that,  therefore,  its  smallness  post-mortem 
was  not  incompatible  w^ith  dilatation  during  life  (see  also 
p.  322). 

Here,  then,  was  a  case  where  the  heart  was  distensible 
to  a  most  remarkable  extent  without  exceeding  the  limit 
of  its  elasticity,  and  so  was  able  to  return  to  its  normal  size 
as  soon  as  the  distending  force  was  removed  by  death  and  its 
contractility  increased  by  rigor  mortis. 

The  ready  distensibility  of  the  heart  in  adolescence  is 
also  very  striking  so  far  as  the  thin  upper  part  of  the  anterior 
wall  of  the  right  ventricle  is  concerned,  and  such  an  observation 
as  the  following  may  easily  be  made.  A  young  woman  of 
seventeen  or  eighteen,  who  is  suffering  from  simple  anaemia 
with  breathlessness,  is  being  examined  in  the  out-patient 
department  of  a  hospital,  and  it  is  found  that  there  is  a 
slight  amount  of  cardiac  dullness  and  pulsation  in  the  second 
left  interspace  suggestive  of  anaemic  dilatation  of  the  conus 
arteriosus  of  the  right  ventricle.  After  the  extent  of  the 
dilatation  has  been  carefully  noted  several  students  are  called 
into  the  room  to  examine  the  patient,  and  it  will  then  not 
infrequently  be  found  that  the  nervous  excitement  caused 
by  their  presence  will,  for  a  time,  greatly  increase  the  amount 
of  the  dilatation.  Or,  to  take  another  instance,  a  young 
man  has  by  over-indulgence  in  athletics  caused  an  over- 
stretching of  the  same  thin  portion  of  the  right  ventricle. 
If  such  a  patient  be  examined  immediately  after  exertion, 
a  much  greater  amount  of  dilatation  of  the  heart  in  the  second 
left  interspace  may  sometimes  be  observable  than  would  be 
found  after  a  few  minutes'  rest. 

Such  observations  as  these  show  that  in  vouth  and  ado- 


ADOLESCENT  TYPE  OF  DILATATION  9 

lescence  the  heart  is  not  only  readily  distensible,  but  also 
possesses  a  high  degree  of  elasticity,  admitting  of  a  rapid  return 
to  its  former  size  as  soon  as  any  abnormal  distensile  strain 
has  lessened. 

This  quality  of  elasticity  is  characteristic  of  adolescence, 
and  is,  as  a  rule,  less  and  less  noticeable  as  the  patient's  age 
increases. 

Type  of  Distensibility  in  Adolescence. — The  heart 
in  adolescence  shows  special  features  as  regards  the  different 
degree  in  which  the  various  parts  of  its  walls  yield  when  there 
is  any  excess  of  internal  pressure.  It  was  pointed  out  at  p.  4. 
that  these  special  features  were  due  to  the  fact  that  the  dis- 
tensibility of  any  particular  part  of  the  heart  wall  appeared 
to  be  proportional  to  its  muscular  weakness  as  compared 
with  the  rest  of  the  heart  wall. 

In  connection  with  the  present  subject  it  is  necessary 
again  to  refer  to  the  comparative  muscular  strength  of  the 
various  portions  of  the  heart  wall. 

In  the  first  place  the  right  ventricle  is  evidently  weaker 
than  the  left,  and  the  relative  strength  of  the  various  parts 
of  its  walls  are  as  follows  :  — 

The  thinnest  part,  and  therefore  the  weakest  muscularly, 
is  the  portion  of  the  anterior  wall  which  lies  nearest  to  the 
pulmonary  artery,  and  includes  the  conus  arteriosus. 

The  next  in  order  of  muscular  strength  is  the  portion 
of  the  anterior  and  right  lateral  walls  which  is  adjacent  to 
the  auriculj-ventricular  orifice. 

The  strongest  portions  are  the  apical  part  with  its  strong 
muscular  bands,  and  the  interventricular  septum. 

As  regards  the  left  ventricle,  the  basal  part  of  its  wall 
which  is  adjacent  to  the  amiculo-ventricular  orifice  is  relatively 
weaker  than  the  apical. 

As  the  strength  of  a  chain  is  that  of  its  weakest  link,  if 
the  ventricle  depended  upon  its  muscular  w^all  alone  for  its 
power  of  resisting  dilatation  due  to  an  abnormal  rise  in  the 
intraventricular  pressure,  the  first  part  of  its  wall  to  give 
way  would  be  the  thinnest  portion. 

Now,  supposing  that  the  resistance  to  be  overcome  in  the 


10  ADOLESCENT  TYPE  OF  DILATATION 

pulmonary  artery  is  raised  to  such  a  degree  that  it  exceeds  the 
resisting  power  of  the  weakest  part  of  the  muscular  wall  of 
the  right  ventricle  but  does  not  exceed  the  strength  of  the 
stronger  portions,  the  intraventricular  pressure  w^ill,  when 
it  reaches  its  maximum,  cause  a  yielding  and  stretching  of 
the  weakest  part  above  named. 

We  can  express  this  in  general  terms  by  saying  that,  in 
such  hearts  as  w^e  are  speaking  of,  when  the  resistance  to  be 
overcome  in  the  pulmonary  artery  exceeds  the  resisting  power 
of  the  weakest  part  of  the  ventricle  wall,  but  does  not  exceed 
the  strength  of  the  strongest  part,  then  the  weaker  parts 
of  the  wall  are  over-distended  by  the  action  of  the  stronger, 
thus  causing  dilatation. 

In  connection  with  this  special  distensibility  of  the  upper 
part  of  the  anterior  w^all  it  must  be  borne  in  mind  that 
the  final  expulsive  efforts  of  the  ventricle  are  concentrated 
on  this  part  of  the  wall  which  lies  nearest  to  the  outlet  ;  for 
in  spite  of  the  physical  law  that  in  any  cavity  containing 
liquid  the  pressure  is  equal  in  all  directions,  the  strain  must 
be  more  prolonged  on  this— the  last  portion  of  the  ventricle 
to  be  emptied. 

What  has  been  said  may  be  summed  up  as  follows  :  — 

In  adolescence,  when,  owing  to  the  softness  and  immaturity 
of  the  fibrous  tissues  the  heart  cannot  rely  on  them  for  support, 
it  requires  but  a  slight  increase  in  the  amount  of  work  the 
heart  has  to  do  to  cause  some  dilatation  of  the  conus  arteriosus 
of  the  right  ventricle,  more  especially  if  the  heart  muscle 
itself  be  lacking  in  tone  from  anaemia  or  other  cause. 

When  the  fibrous  tissues  become  less  elastic,  in  middle 
and  later  life,  the  right  ventricle  not  only  loses  its  ready 
dilatabiiity,  but  its  type  of  dilatation  changes  also  ;  for  the 
conus  arteriosus  no  longer  shows  the  special  weakness  that 
it  does  in  earlier  hfe,  and,  under  these  circumstances,  w'e 
find  that  the  first  part  of  the  ventricle  to  yield,  when  over- 
strained, is  the  basal  portion  of  the  anterior  and  right 
lateral  wall  in  general,  and  not  the  small  portion  below  the 
pulmonary  valves. 

This  increase  in  the  strength  of  the  wall  of  the  right  ventricle 
in  middle  and  later  life  is  natm'ally  associated  with  a  relatively 


ADOLESCENT  TYPE  OF  DILATATION  11 

increased  frequency  in  the  occurrence  of  dilatation  of  the 
left  ventricle,  as  the  result  of  overstrain. 

In  adolescence,  when  the  heart  is  overstrained,  early  failure 
of  the  weak  right  ventricle  saves  the  left  from  dilatation.  In 
adult  life  it  is  usual  to  find  the  left  ventricle  at  least  as  much 
dilated  as  the  right,  and  when  the  fibrous  tissues  have  become 
relatively  rigid,  we  may  find  dilatation  of  the  left  side  more 
extensive  than  that  of  the  right.  This  will  be  referred  to  again, 
later  on,  in  speaking  of  failure  of  the  left  ventricle. 

The  special  distensibility  of  the  conus  arteriosus,  therefore, 
is  found  to  diminish  as  the  fibrous  strength  of  the  heart  and 
pericardium  increase  with  advancing  years  ;  and  although 
the  period  of  life  when  the  change  takes  place  varies  very 
much  in  different  individuals  it  is  fairly  safe  to  say  that  the 
special  dilatability  of  the  conus  arteriosus  is  lost  as  a  rule 
towards  the  end  of  the  third  decade  ;  and  in  patients  over 
thirty-five  it  is  not  common  to  find  failure  of  the  right  ventricle, 
from  overstrain  or  other  cause,  accompanied  by  the  dilatation 
upwards  and  to  the  left  which  characterises  a  yielding  of  the 
conus  arteriosus.  In  such  patients  the  dilatation  will  most 
commonly  be  a  general  one  of  the  base  of  the  right  ventricle, 
and  the  enlargement  of  the  heart  will  be  to  the  right  rather 
than  upwards  and  to  the  left.  This,  which  may  well  be  called 
the  adult  type  of  dilatation,  may  sometimes  occur  in  patients 
much  younger  than  the  age  above  mentioned,  and,  on  the 
other  hand,  the  adolescent  type  may  sometimes  be  found  in 
patients  well  over  fifty  years  of  age. 

Certain  conditions  of  ill-health,  however,  appear  to  be 
accompanied  by  a  tendency  to  softening  of  the  fibrous  elements 
of  the  heart  walls,  thus  increasing  their  distensibihty  :  this 
is  notably  the  case  with  rheumatic  fever.  After  a  severe 
attack  of  rheumatism,  when  the  patient  first  begins  to  get 
up,  the  conus  arteriosus  will  often  be  found  to  dilate  far 
more  readily  on  slight  exertion  than  would  be  the  case  after 
such  an  illness  as  pneumonia.  It  is  possible  that  this 
softening  effect  of  rheumatism  is  of  value  in  allowing  the 
necessary  compensatory  dilatation  to  take  place  in  mitral 
and  aortic  regurgitation,  and  is  therefore  to  that  extent 
beneficial.      When   a  case  of  aortic    or  mitral  regurgitation 


12  ADOLESCENT  TYPE  OF  DILATATION 

occurs  in  a  patient  whose  heart  walls  are  too  rigid  to  admit 
of  compensatory  dilatation,  it  shows  what  a  serious  thing 
such  valvular  disease  would  prove  to  be,  were  it  not  for 
the  ready  distensibility  of  the  heart  walls  in  most  of  the 
patients  who  suffer  from  rheumatic  endocarditis  {vide  Essay 
on  Pallor,  p.  448). 

After  an  attack  of  rheumatism,  or  some  allied  ailment, 
it  may  be  found  that  in  a  patient  over  thirty  the  conus 
arteriosus  seems  to  be  as  dilatable  as  in  a  normal  patient 
of  twenty  or  twenty-five  years  of  age. 

Early   Diagnosis  of   Heart  Failure  with   Enlargement 
IN  Distensible  Hearts 

After  what  has  just  been  said  as  to  the  relative  strength 
of  the  right  and  left  sides  of  the  heart  in  early  life,  it  will  be 
recognised  that  the  early  diagnosis  of  heart  failure  \vdth  en- 
largement in  early  life  is  simply  the  early  diagnosis  of  dilatation 
of  the  right  ventricle.  It  has  already  been  pointed  out  that 
dilatation  of  the  right  ventricle  in  early  life  shows  itself  first 
as  an  upward  and  outward  dilatation  of  the  part  of  the  anterior 
wall  which  lies  just  below  the  pulmonary  valves,  and  therefore 
it  is  to  the  symptoms  and  physical  signs  of  tliis  type  of  dilatation 
that  we  must  look  for  the  earliest  indication  of  failure  in  a 
distensible  heart. 

Symptoms. — The  early  signs  and  symptoms,  which  are 
characteristic  of  this  condition,  will  first  be  discussed,  and  then 
subsequently  their  relative  order  of  occurrence  and  their 
diagnostic  importance. 

Dyspnoea  is  in  this,  as  in  all  cases  of  cardiac  failure,  one 
of  the  earhest  indications  that  the  heart  is  unequal  to  the  work 
it  has  to  do. 

The  breathlessness  of  right  ventricular  f  ailm-e  in  adolescence 
has,  however,  some  special  characteristics. 

In  the  first  place  its  amount  is  often  very  gi'eat,  especially 
when  associated  with  anaemia,  as  is  so  commonly  the  case. 

When  right  ventricular  failure  accompanies  a  severe  ansemia, 
the  breathlessness  may  be  so  great  that  the  patient  cannot 
go  up  more  than  three  or  fom-  steps  without  stopping  to  rest. 


SYMPTOMS  13 

Such  an  amount  of  dyspnoea  under  other  circumstances 
would  mean  serious  organic  disease  of  the  heart,  but  in  the 
case  of  dilatation  of  the  right  ventricle  in  an  antemic  adolescent 
a  few  weeks  of  rest,  and  the  administration  of  iron,  will  often 
^suffice  to  restore  the  working  power  of  the  heart. 
/  A  special  characteristic  of  the  breathlessness  associated 
with  this  adolescent  type  of  heart  failure  is  the  well-known 
tendency  to  take  deep  sighing  breaths.  These  respirations 
consist  of  a  full  inspiration  which  is  held  as  in  an  ordinary 
sigh,  although  for  a  slightly  longer  time,  and  then  the  air  in 
the  chest  is  suddenly  allowed  to  escape. 

This  type  of  respiration  gives  distinct  relief  in  this  kind 
of  case. 

The  physiological  basis  for  this  fact  may  for  the  sake  of 
completeness  be  referred  to  here. 

When  the  right  ventricle  is  somewhat  over-burdened  and 
has  a  difficulty  in  expelling  its  contents,  owing  to  the  abnormal 
resistance  in  the  pulmonary  artery,  the  long  and  powerful 
inspiration  has  the  effect  of  drawing  an  extra  amount  of  blood 
into  the  great  veins  and  the  right  heart.  The  breath  is 
presumably  held  until  such  time  as  the  commencement  of 
expiration  coincides  with  the  contraction  of  the  ventricle.  As 
a  result  of  this,  the  expiratory  increase  in  the  intra-thoracic 
pressure  comes  at  the  right  time  to  give  some  measure  of  support 
to  the  weak  and  stretching  walls  of  the  right  ventricle,  thus 
aiding  its  expulsive  power  and  also,  by  increasing  the  external 
pressure  upon  the  veins  and  auricle,  lessening  the  tendency 
to  tricuspid  leakage,  if  there  be  any,  and  helping  the  subsequent 
filling  of  the  ventricle. 

Clinical  proof  can  easily  be  obtained  that  the  expiratory 
increase  of  intrathoracic  pressure  does  materially  aid  the 
heart's  action  in  this  type  of  heart  failure. 

Thus  in  cases  where  the  pulsation  of  the  right  ventricle 
is  visible  in  the  third  and  second  left  interspaces  (p.  18), 
it  can  be  seen  that  the  first  sj^stole  after  the  commencement 
of  expiration  causes  a  larger  wave  of  pulsation  than  other 
beats. 

Also  where  accurate  means  are  adopted  {vide  p.  413)  of 
measuring  the  loudness  of  the  heart  sounds  it  is  often  noticeable 


14  ADOLESCENT  TYPE  OF  DILATATION 

that  the  first  pulmonary  second  sound  to  occur  after  the  end 
of  insphation  is  louder  than  the  others.  Further,  in  the  case 
of  murmurs  produced  by  the  action  of  the  right  ventricle  it 
is  often  noticeable  that  they  are  louder  at  the  commencement 
of  expiration  than  during  the  remainder  of  the  respiratory 
cycle. 

This  taking  of  a  long  breath  is  common  in  all  cases  of  right 
ventricular  failure  in  distensible  hearts,  but  especially  so  where 
there  is  anaemia  as  well. 

The  relief  it  gives  is  so  well  known  to  the  patients  them- 
selves that,  when  the  heart  gets  worse  and  the  same  relief 
is  no  longer  obtainable,  they  will  sometimes  answer  the  doctor's 
question  '  What  do  you  complain  of  ?  '  by  saying  '  I  can't 
take  the  long  breath.' 

Before  speaking  of  the  physical  signs  observable  in  this 
type  of  heart  failure  it  will  be  well  to  say  a  word  or  two  as 
to  certain  other  symptoms  of  heart  failui'e  from  which  patients 
suffer. 

Pain. — Occasionally  a  certain  amount  of  discomfort  or 
dull  pain  can  be  felt  over  the  situation  of  the  dilated  conus 
arteriosus,  and  in  some  patients  this  sense  of  discomfort 
precedes  the  occm-rence  of  breathlessness  and  tells  the  patient 
that  the  exertion  which  is  being  taken  is  overtaxing  the 
heart. 

Globus  hystericus. — A  less  common  symptom  is  that  of  a 
lump  in  the  throat,  as  if  too  large  a  bolus  of  food  had  been 
swallowed  and  was  lodged  in  the  lower  end  of  the  oesophagus. 
This  sensation  is  possibly  due  to  the  pressm-e  of  an  over- dis- 
tended left  auricle  upon  the  oesophagus  in  a  sensitive  patient. 
I  have  only  met  with  it  in  the  distensible  hearts  of  adolescence, 
but  it  may  occur  in  other  conditions. 

Clinical  Phenomena  Associated  with  the  Veins. — 
Pulsation  in  the  veins  of  the  neck. — One  of  the  earliest 
symptoms  of  this,  as  of  other  types  of  right  ventricular 
failure,  is  the  undue  fullness  of  the  veins  of  the  neck, 
which  results  from  the  difficulty  which  the  right  ventricle 
experiences  in  forwarding  the  blood  through  the  lungs  at 
the  normal  rate. 


PHYSICAL  SIGNS  15 

At  first  a  simple  fullness  of  the  veins  is  observable.  Later, 
when  the  delay  is  greater,  a  distinct  variation  in  their  fullness 
can  be  detected,  and  the  character  of  the  variation  is  dependent 
both  upon  respiratory  and  upon  cardiac  movements. 

The  respiratory  variation  consists  in  an  increased  fullness 
during  expiration  and  a  relative  emptying  of  the  veins  during 
inspiration. 

This  respiratory  rhythm  is  superimposed  upon  the  variation 
due  to  the  heart.  This  double  variation  is  known  as  false 
PULSATION  in  the  neck  veins. 

The  cardiac  variation  in  early  cases  of  failure  consists  in 
what  is  apparently  a  systolic  filHng  of  the  veins.  On  closer 
examination,  however,  it  can  easily  be  recognised  as  the  type 
of  pulsation  which  is  not  a  true  but  a  false  venous  pulsation. 
In  this  type,  the  variation  consists  in  a  rhythmical  emptying  of 
veins  that  are  unduly  distended  and  not  in  a  rhythmical  filling 
of  veins  that  are  relatively  empty — such  as  occurs  in  tricuspid 
regurgitation.  Proof  of  this  is  given  by  the  fact  that  the 
pulsation  is  apt  to  be  more  marked  and  distmct  during 
inspiration  than  dm-ing  expiration — that  is  to  say,  the 
amount  of  cardiac  variation  in  the  fullness  of  the  veins  is 
increased  by  anything  aiding  the  entrance  of  blood  into  the 
heart.  In  true  tricuspid  regm-gitation  the  reverse  condition  is 
found,  for  the  pulsation,  where  it  varies  at  all  with  respiration, 
is  always  more  distinct  during  expiration  than  dm-ing  inspira- 
tion ;  for  the  escape  of  blood  from  the  heart  into  the  veins  is 
favoured  during  expii-ation,  whereas  inspiration  tends  to  hinder 
it.  Associated  with  this  false  pulsation,  which  characterises 
cases  of  right  ventricular  failure  where  there  is  no  marked 
tricuspid  regm-gitation,  we  find,  under  certain  conditions,  a 
definite  venous  hum  or  murmur,  most  marked  in  anaemic 
states,  and  commonly  known  as  the — 

'  Bruit   de   Diable.' 

This  murmur,  as  is  well  known,  is  due  to  the  fact  that 
when  the  neck  veins  are  over-distended  there  are  certain  points 
where  they  receive  enough  external  support  fi'om  the  fascia, 
&c.,  to  prevent  them  from  dilating,  and  thus  constrictions 
are  formed  where  murmurs  can  arise.  If  the  veins  be  over- 
distended  with  hard  parafl&n,  it  will  be  found  that  a  constriction 


16  ADOLESCENT  TYPE  OF  DILATATION 

occui's  wherever  a  small  vein  joins  a  larger  one,  owing  to  the 
support  received  by  the  small  vein  at  its  point  of  entrance 
into  the  wall  of  the  larger  one.  The  orifice  of  entrance,  there- 
fore, of  the  smaller  vein  does  not  dilate  to  the  same  extent  as 
the  vein  itself  does. 

This  murmm",  which  is  low-toned  and  humming,  is  found 
to  vary  in  tone  with  both  the  respiratory  and  the  cardiac 
rhythm,  and  in  moderately  severe  cases  it  disappears  entirely 
when  the  patient  lies  down.  This  is  due  probably  to  the  fact 
that  in  the  recumbent  attitude  the  veins  in  the  clavicular 
region  are  less  distended,  owing  to  the  elimination  of  the  action 
of  gravity.  In  confijmation  of  this  it  may  be  noticed  that 
on  lying  down  the  veins  in  the  upper  part  of  the  neck  become 
more  distended  than  they  are  when  the  patient  is  erect.  This 
variation  in  the  fullness  of  the  veins  is  specially  noticeable 
where  there  is  the  poor  venous  and  cardiac  tone  which  char- 
acterises cases  showing  a  '  bruit  de  diable.' 

True  Pulsation  in  the  neck  veins. — The  true  systolic 
venous  pulsation,  which  characterises  tricuspid  regurgitation, 
is  easily  distinguished  from  this  false  pulsation  with  which 
we  have  just  dealt.  True  venous  pulsation  does  not,  as  a 
rule,  occur  with  the  type  of  cardiac  failure  of  which  we  are 
now  speaking. 

The  dilatation  of  the  conus  arteriosus  is  due,  as  already 
pointed  out,  to  a  rise  in  the  systolic  ventricular  pressure  beyond 
the  point  that  the  muscular  walls  can  stand.  Such  a  rise 
in  the  interventricular  pressm-e  implies  either  a  competent 
tricuspid  valve  or  else  a  degree  of  auricular  and  venous  tonic 
contraction  sufficient  so  far  to  limit  the  tricuspid  regurgitation 
as  to  make  possible  a  rise  in  the  intraventricular  pressure 
above  its  normal  level.  In  adolescence,  however,  such  strength 
in  the  musculature  of  the  veins  and  amicle  is  not  to  be  expected, 
and  therefore  we  do  not  expect  to  find  tricuspid  regurgitation 
associated  with  upward  dilatation  of  the  ventricle  as  an  early 
sign  of  heart  failure  in  distensible  hearts. 

In  severe  cases,  however  (especially  in  those  where  the 
failure  of  the  right  ventricle  is  secondary  to  valvular  disease  of 
the  left),  marked  dilatation  upwards  may,  even  in  distensible 
hearts,   be   accompanied   by   some   general   dilatation  of  the 


PHYSICAL  SIGNS  17 

right  ventricle,  auricle,  and  veins  such  as  characterises  heart 
failure  in  adult  and  later  life. 

The  subject  of  true  systolic  pulsation  in  the  veins  of  the 
neck  may  therefore  be  deferred  until  cardiac  failure  in  less 
distensible  hearts  is  dealt  with. 

Physical  Signs. — The  chief  physical  signs  upon  which  we 
have  to  rely  for  the  early  recognition  of  heart  failure  in 
distensible  hearts  are  due  to  the  special  direction  in  which 
such  hearts  dilate — namely,  upwards  and  to  the  left,  in 
consequence  of  the  yielding  of  the  thin  part  of  the  right 
ventricle. 

Inspection  of  the  Heart. — One  of  the  first  signs  of  failure 
of  a  distensible  right  ventricle  is  the  appearance  of  pulsation 
at  the  sternal  end  of  the  fourth  left  interspace,  or  its  increase 
in  amount  if  it  have  been  previously  present  there. 

With  increasing  dilatation,  pulsation  will  appear  in  the 
third  left  interspace,  and,  subsequently,  in  the  second,  if 
the  right  ventricular  dilatation  be  considerable.  In  such  a 
case  there  will  be  visible  pulsation  in  the  second,  third,  and 
fourth  interspaces,  and  it  may  extend  from  the  left  edge 
of  the  sternum  to  the  vertical  nipple  line  in  the  second  left 
space,  and  may  sometimes  reach  to  the  anterior  axillary 
line  in  the  third  and  fourth.  In  such  a  marked  case  there 
will  be  so  much  of  the  right  ventricle  uncovered  by  lung 
tissue  that  the  character  of  the  pulsation  will  be  clearly 
distinguishable. 

The  presence  of  this  pulsation  was  first  described,  I  believe, 
by  the  late  Dr.  Foxwell  in  his  Cambridge  graduation  thesis, 
and  subsequently  in  his  '  Bradshaw  Lecture '  and  his  '  Essays 
in  Heart  and  Lung  Disease.' 

Its  features  are  quite  characteristic.  It  has  a  fluttering 
^.ppearance,  and  is  not  the  simple  rise  and  fall  such  as  is  seen, 
for  instance,  in  aneurysm.  This  irregularity  is  due  to  its 
variation  with  respiration,  and  also  to  the  fact  that  it  has  a 
sort  of  wave-like  motion :  the  line  of  maximal  rise  travelling 
from  one  side  of  the  pulsating  area  to  the  other  like  an 
ordinary  wave-crest  on  water. 

The  respiratory  variation  consists  in  a  greater  degree  of 


18  ADOLESCENT  TYPE  OF  DILATATION 

visible  movement  during  expiration  than  during  inspiration. 
This  will  at  first  be  thought  to  be  due  to  the  heart  being  less 
covered  by  the  lungs  during  their  expiratory  recession  ;  but  on 
making  the  patient  hold  the  breath  with  the  lungs  fully 
emptied  it  is  found  that  the  pulsation  is  less  than  it  is 
during  the  continuance  of  ordinary  respiration. 

If  the  pulsation  be  still  more  carefully  watched  it  can 
usually  be  noticed  that  the  maximal  degree  of  pulsation 
occurs  with  the  first  cardiac  systole  which  follows  the  end  of 
inspiration,  and  sometimes  the  systolic  impulse  with  this  beat 
is  decidedly  greater  than  that  due  to  the  other  heart  beats. 

The  other  characteristic  of  this  right  ventricular  pulsation 
is  the  visible  passage  of  the  wave  of  contraction  across  the 
pulsating  area. 

Considering  that  the  blood  is  being  emptied  out  of  the 
ventricle  through  an  orifice  (the  pulmonary  artery)  which 
lies  under  the  second  rib  and  some  one  inch  or  more  to  the 
left  of  the  sternum,  it  might  be  expected  that  the  peristaltic 
wave  would  be  seen  passing  up  from  the  apex  and  gaining 
in  volume  and  distinctness  as  it  approached  the  pulmonary 
artery — as  is  the  case  with  the  muscular  wave  which  causes 
the  emptying  of  the  stomach. 

The  direction  of  the  muscular  movement  in  the  right 
ventricle  has,  however,  quite  a  different  direction  from  this.  It 
first  appears  travelling  out  from  under  the  sternum  in  the 
second  or  third  interspace  and  travels  downwards  and  outwards 
over  the  exposed  part  of  the  right  ventricle  more  or  less 
parallel  to  the  line  of  the  auriculo-ventricular  groove,  though 
inclined  rather  more  downwards,  and  also  more  or  less  parallel 
to  the  direction  of  the  pulmonary  artery. 

The  line  of  crest  runs  in  a  straight  not  a  curved  hne,  and 
its  direction  of  movement  is  a  Hne  inclined  some  thirty  degrees 
to  the  vertical,  whereas  that  of  the  auriculo-ventricular 
septum  would  be  more  nearly  vertical,  say,  vdtli  an  inclination 
of  some  twenty  degrees  or  less.  The  direction  of  this  wave 
seems  compatible  with  modern  myogenic  theory  as  to  the 
origin  of  the  stimulus  to  contraction. 

The  other  points,  wliich  may  be  gathered  by  inspection 
of  the  cardiac  area,  are  the  absence  of  pulsation  to  the  right 


TYPE  OF  CARDIAC  PULSATION  19 

of  the  sternum,  owing  to  the  limitation  of  the  dilatation  to  the 
portion  of  the  anterior  wall  near  the  pulmonary  valves  and 
also  the  abnormal  position  of  the  apex  beat,  wliich  will  be 
fm-ther  referred  to  when  dealing  with  palpation,  and  which 
is  also  fully  discussed  at  p.  348. 

Palpation. — Study  of  the  cardiac  impulse  by  palpation 
confirms  the  supposition  (based  on  its  respiratory  variations 
and  other  characteristics)  that  it  is  due  to  the  right  ventricle. 
It  is  not  a  powerful  pulsation  like  that  of  the  left  ventricle, 
and  is  better  studied  by  inspection  than  by  palpation. 

Palpation  is,  however,  of  great  value  as  a  quick  and  simple 
means  of  detecting  the  presence  of  this  type  of  dilatation  of 
the  right  ventricle ;  for  the  occurrence  of  true  cardiac  pulsa- 
tion in  or  external  to  the  nipple  line  in  the  third  interspace 
is  (allo^ving  for  the  uncertainties  common  to  all  medical  state- 
ments) pathognomonic  of  this  condition.  The  presence  or 
absence,  therefore,  of  upward  dilatation  can,  when  well  marked, 
be  easily  determined  by  careful  palpation,  Avith  the  tip  of  one 
finger,  in  this  situation.  If  pulsation  be  felt,  dilatation  of  the 
conus  arteriosus  of  the  right  ventricle  can  be  diagnosed,  and  if 
there  be  no  pulsation  in  this  situation  it  is  almost  equally 
certain  that  there  is  no  dilatation. 

Before  making  this  diagnosis,  however,  the  absence  of 
marked  displacement  of  the  heart  from  disease  of  one  or  other 
lung  must  be  excluded. 

Another  fact  to  be  looked  for  by  palpation  is  the  altered 
position  of  the  apex  beat.  Often  in  these  cases  the  cardiac 
apex  is  higher  than  normal,  being  found  in  the  fourth  inter- 
space instead  of  the  fifth,  and  is  also  external  to  its  proper 
situation.  In  well-marked  cases  the  heart's  apex  may  be 
in  the  fourth  interspace,  well  outside  the  vertical  nipple  line, 
and  sometimes  not  far  from  the  anterior  axillary  line. 

The  causes  at  work  producing  this  change  are  discussed 
fully  at  pp.  234  and  348,  to  which  the  reader  is  referred. 

The  presence  of  a  palpable  thrill  over  the  pulmonary 
artery  may  be  detected  in  severe  cases  of  this  type,  but  more 
especially  where  upward  dilatation  of  the  right  ventricle  is 
associated  with  ansemia. 

Percussion  of  the  Heart   in   adolescent    dilatation  of 


20  THEORY  OF  PERCUSSION 

the  right  ventricle. — Percussion  is  as  valuable  as  palpation 
in  determining  the  presence  or  absence  of  this  type  of  dilatation, 
but  does  not  take  the  premier  place  as  a  diagnostic  method 
because,  as  a  rule,  the  cardiac  vigour  which  is  necessary  for 
the  development  of  dilatation  \vill  also  ensure  the  presence  of 
an  amount  of  pulsation  which  can  be  recognised  by  palpation. 

By  percussion,  however,  the  exact  size  and  shape  of  the 
cardiac  area  can  be  determined  in  greater  detail  than  by 
palpation. 

Before,  however,  going  further  with  this  subject  it  ^yi\l 
be  well  to  say  a  few  words  upon  the  question  of  percussion 
in  general — more  especially  because  a  good  deal  of  the  clinical 
evidence  advanced  in  support  of  the  theories  here  propounded 
is  based  on  the  results  of  percussion. 

The  Principles  and  Method  of  Percussion 

First  as  to  method.  The  finger  as  pleximeter  has  many 
advantages  over  any  artificial  substitute,  and  not  the  least 
of  these  is  the  information  gained  by  the  resistance  offered 
by  a  solid  or  partially  solid  organ  underlying  it,  as  compared 
with  an  air- containing  one.  So  much  is  this  the  case  that 
it  is  possible  for  the  inexperienced  percusser,  when  suffering 
from  the  usual  periosteal  irritation  which  results  from  too 
much  enthusiasm  in  the  newly  acquired  art,  to  tell  by  the 
varying  degrees  of  pain  caused  by  the  percussion  stroke  the 
degree  of  density  of  the  organ  percussed. 

The  plessor,  too,  had  better  be  the  finger  of  the  clinician 
rather  than  a  hammer  of  any  sort,  for  the  finger  is  capable 
of  a  far  quicker  blow  than  any  hammer,  and  the  clearness  of 
the  percussion  note  is  dependent  upon  the  quickness  of  the 
blow  whatever  its  force  may  be.  A  sustained  blow  cannot  fail 
to  check  the  fullness  of  the  vibration  to  which  the  percussion 
stroke  gives  rise. 

As  to  the  most  useful  of  the  two  kinds  of  percussion,  there 
is  no  need  to  raise  the  old  controversy  as  to  which  is  the  best 
mode — whether  gentle  or  strong  ;  for  the  use  of  both  kinds 
gives  us  such  valuable  information  that  we  cannot  aft'ord  to 
discard   either.     We   have   need   to   observe    both   the   area 


THEORY  OF  PERCUSSION  21 

where  the  dullness  of  a  solid  organ  is  complete,  as  well  as  the 
area  where  that  dullness  is  modified  by  the  presence  above 
or  below  it  of  a  resonant  air-containing  viscus. 

As  to  terminology,  it  would  be  an  advantage  if  the  terms 

*  absolute  '  and  *  relative '  dullness,  or  some  equally  unmis- 
takable ones,  were  generally  adopted  instead  of  the  more 
equivocal  terms  '  superficial '  and  *  deep  '  dullness.  Some 
medical  wiiters  seem  to  use  these  latter  terms  in  opposite 
senses,  and  it  certainly  is  possible  to  take  the  term  '  deep  ' 
dullness  to  apply  to  the  fully  dull  note  of  a  solid  organ  at  the 
surface,  as  well  as  applying  to  the  note  of  a  dull  organ  lying 
deeply.  Another  disadvantage  in  the  use  of  the  term  superficial 
dullness  is  that  a  solid  organ,  although  superficial,  may 
give  only  a  relatively  dull  note  ('  deep  dullness  ')  if  underlaid 
by   a   resonant    organ.     In    the    following    pages   the   terms 

*  absolute '  and  '  relative  '  will  be  used,  and  they  have  the  ad- 
vantage of  being  also  serviceable  in  describing  the  resonance 
of  such  an  organ  as  the  stomach  or  colon,  the  absolute  resonance 
being  the  full  resonance  obtainable  when  the  percussion  note 
is  not  damped  by  any  superimposed  solid  organ  ;  and  the 
relative  resonance  being  the  partial  resonance  obtainable 
when  the  liver,  or  other  intervening  solid  tissue,  modifies 
the  amplitude  of  the  note. 

In  the  illustrations  which  show  the  results  of  percussion, 
the  absolute  dullness  will  be  marked  by  dark  shading,  and 
the  relative  dullness,  whether  due  to  the  presence  of  an  air- 
containing  organ  overlying  or  underlying  the  dull  one,  will  be 
marked  by  lighter  shading. 

As  regards  the  information  gained  by  percussion. 

Firstly,  take  the  case  of  a  dull  organ  which  is  overlaid  in 
part  by  an  air-containing  one,  such,  for  instance,  as  the  upper 
border  of  the  liver  and  the  upper  and  outer  border  of  the 
normal  heart,  where  they  come  into  relationship  with  the 
lungs.  Here,  by  very  light  percussion,  we  endeavour  to  map 
out  the  exact  edge  of  the  lung,  calling  the  area  uncovered  by 
lung  the  absolute  dullness  of  the  liver  or  heart  respectively. 
In  the  same  way,  by  stronger  percussion,  we  endeavour  to 
define  the  area  over  which  some  damping  of  the  full  lung  note 
can  be  recognised  (owing  to   the  presence  of  the  underlying 


22  THEORY  OF  PERCUSSION 

solid  organ),  and  wc  call  this  area  the  relative  dullness  of  the 
liver  or  heart  respectively :  though  we  should  be  equally 
accurate  in  calling  it  the  area  of  relative  lung  resonance.  The 
width  to  which  this  area  of  relative  dullness  is  found  to 
extend  around  the  area  of  absolute  dullness  naturally  depends 
to  some  extent  upon  the  skill  of  the  observer  and  the  depth 
of  lung  tissue  which  he  is  able  to  cause  to  vibrate  as  the  result 
of  his  percussion  stroke.  The  less  effective  stroke  failing  to 
reveal  the  presence  of  the  dull  organ  at  so  great  a  depth  as  the 
more  effective  one. 

This  variation  in  the  boundary  of  the  relative  dullness, 
according  to  the  skill  displayed,  has  been  advanced  as  an 
argument  against  the  clinical  value  of  recording  the  relative 
dullness.  But  the  variation  due  to  this  personal  equation  is 
not  great  enough  to  give  much  force  to  this  argument. 

The  movement  of  the  edge  of  the  lung  during  respiration 
must  naturally  be  taken  into  consideration,  and  for  very 
exact  records  it  is  necessary  that  the  breath  be  held  in  the 
middle  of  expiration  or  inspiration.  In  the  figures  given  in 
the  following  pages  the  line  is  the  average  level — unless 
otherwise  stated. 

In  determining  the  area  of  the  relative  dullness  it  must 
not  be  forgotten  that  mobility  of  the  lungs  is  of  value  in  con- 
firming the  line  which  is  decided  upon  as  marking  the  boundary 
of  the  relative  dullness.  By  percussing  again,  when  the  patient 
has  fully  emptied  the  lungs,  the  correctness  or  otherwise  of 
the  previous  observation  can  easily  be  verified. 

It  has  previously  been  stated  that  the  observation  of  both 
the  absolute  and  the  relative  dullness  of  an  organ  gives  valuable 
information.  Let  the  upper  level  of  the  liver  anteriorly  be 
taken  as  an  example.  To  note  the  situation  of  the  absolute 
or  of  the  relative  dullness  alone  gives  simply  the  approximate 
position  of  the  upper  level  of  the  liver.  If,  however,  both  are 
noted,  it  is  possible  to  estimate  the  rate  at  which  the  liver  is 
receding  from  the  surface — or,  in  other  words,  the  rapidity  with 
which  the  lower  edge  of  the  lung  thickens.  The  narrower 
the  band  of  relative  dullness  which  intervenes  between  the 
full  resonance  of  the  lung  and  the  full  dullness  of  the  liver 
the  more  sudden  must  be  the  recession  of  the  diaphragm 


THEORY  OF  PERCUSSION  23 

and  liver  from  the  chest  wall,  and  the  broader  the  relative 
dullness  the  more  gi'adual  that  recession. 

In  this  way  it  is  often  possible  to  estimate  the  degree  of 
arching  of  the  diaphragm.  If  the  breadth  of  the  area  of 
relative  dullness  exceeds  the  normal  it  suggests  that  the 
diaphragm  is  abnormally  arched.  If  less  than  the  normal, 
that  it  is  either  unduly  flat  or  else  that  the  edge  of  the  lung 
is  distended  in  the  manner  that  occm-s  in  emphysema. 

The  broad  zone  of  relative  dullness  which  suggests  abnormal 
arching  of  the  diaphragm  is  well  shown  in  fig.  31,  p.  174. 

Secondly,  where  a  dull  organ  is  underlaid  by  a  resonant 
one  the  method  of  procedure  must  be  reversed,  so  far  as  the 
area  of  the  dullness  of  the  organ  is  concerned ;  for  its  area  of 
absolute  dullness  must  be  determined  by  strong  percussion, 
and  the  boundary  of  its  area  of  relative  dullness  by  light  per- 
cussion. This  is  best  illustrated  by  the  percussion  of  the  lower 
edge  of  the  liver,  where  it  overlies  the  resonant  stomach  or 
intestines.  It  requires  a  gentle  stroke  to  define  the  thin  edge 
of  the  Hver,  where  it  lies  over  the  resonant  stomach,  and  a 
stronger  blow  to  elicit  the  resonance  of  the  stomach  or  bowel 
when  it  underlies  some  thickness  of  liver  tissue.  To  define 
the  absolute  dullness  here  requires  therefore  a  strong  stroke, 
and  to  define  the  relative  dullness  a  gentle  one.  Informa- 
tion of  clinical  importance  can  be  obtained  by  noting  the 
lower  boundary  of  the  liver  dullness  through  a  series  of 
cases;  for  it  shows  gi-eat  variation,  and  in  cases  of  defective 
circulation  there  may  be  very  gi'eat  diminution  in  the  area 
usually  occupied  by  the  dullness  of  the  lower  part  of  the  liver. 
This  subject  is  discussed  in  the  Essay  on  Diminution  of  the 
Liver  Dullness,  at  p.  185. 

These  two  methods  of  obtaining  the  absolute  dullness 
of  the  liver  may  be  harmonised  and  embraced  by  a  single 
generalisation  as  follows  : — 

In  defining  by  percussion  the  boundary  between  an  organ 
giving  a  dull  percussion  note  and  one  giving  rise  to  a  resonant 
note,  the  boundary-Hne  along  which  the  underlying  one  comes 
to  the  surface  must  be  determined  by  light  percussion,  and  the 
farthest  point  where  its  note  can  be  detected  through  the 
overlying   one    by   strong   percussion.     In    other  words,  the 


24  THEORY  OF  PERCUSSION 

absolute  dullness  or  absolute  resonance  of  the  underlying  organ 
must  be  obtained  by  light  percussion,  and  its  relative  dullness  or 
resonance  by  strong  percussion — e.g.,  the  lower  edge  of  the  Hver 
when  marking  the  limit  of  full  intestinal  or  gastric  resonance 
needs  light  percussion,  the  lower  border  of  the  absolute  hepatic 
dullness,  marking  the  upper  limit  of  the  relative  or  partial 
gastric  (or  intestinal)  resonance,  needs  strong  percussion. 

A  further  generalisation  is  also  in  the  main  accurate — 
namely,  that  the  rate  at  which  the  underlying  organ  is  receding 
fi'om  the  surface  may  be  inferred  fi'om  the  width  of  the  area 
which  hes  between  these  two  boundary-lines — i.e.,  of  the  area 
of  relative  dullness.  The  nearer  these  lines  are  together  the 
steeper  the  angle  at  which  it  is  receding,  and  the  farther 
they  are  apart,  the  less  the  angle,  and  the  more  gradual  the 
recession. 

While  speakmg  on  the  subject  of  percussion  it  may  be  well 
to  draw  attention  to  a  fm'ther  point,  which  will  be  of  importance 
in  a  subsequent  essay  (see  p.  191),  although  it  does  not  concern 
the  present  one.  This  point  is  that  this  last-named  generalisa- 
tion does  not  always  seem  to  hold  good  so  far  as  the  lower  edge 
of  the  liver  is  concerned,  for  under  certain  circumstances  a 
diminution  in  the  amount  of  liver  dullness  in  the  right  hypochon- 
drium  does  not  always  seem  to  be  due  to  a  lessening  of  the 
amount  of  liver  substance  that  intervenes  between  the  point 
percussed  and  the  resonant  intestines  underneath.  Some- 
times the  edge  of  the  liver  can  be  clearly  felt  at,  or  below, 
its  normal  situation  when  the  area  over  which  the  full  intestinal 
resonance  is  obtainable  on  percussion  extends  far  above  its 
normal  limits  ;  thus  suggesting  that  the  intestinal  resonance 
must  in  this  case  be  obtainable  through  a  far  thicker  mass 
of  liver  tissue  than  is  normally  possible. 

There  is,  I  think,  no  doubt  that  under  certain  pathological 
conditions  the  liver  tissue  loses  its  power  of  damping  down 
percussion  vibrations. 

The  subject  is,  however,  one  needing  further  research,  and 
it  will  probably  be  found  that  the  possession  of  this  quality  is 
a  sign  that  the  liver  tissue  is  unduly  tense  through  congestion 
(or  unduly  hard),  and,  therefore,  has  the  power,  when  distended 
bowel  is  in  close  contact  with  it,  of  conducting  the  vibrations 


PERCUSSION  OF  THE  HEART  25 

of  the  percussion  stroke  to  the  bowel,  and  the  vibrations  of 
the  bowel  wall  back  to  the  surface. 

It  is  quite  probable  that  the  possession  by  the  liver  of 
this  increased  power  of  conducting  percussion  vibrations 
may  prove,  when  fully  investigated,  as  valuable  a  sign  of 
congestion  or  hardening  of  the  liver  substance  as  the  power 
of  conducting  aerial  \abrations  has  proved  to  be  in  the  case 
of  consolidation  of  the  lung  (see  also  pp.  189-193). 

The  occurrence  of  such  unexpected  percussion  results  as 
this  in  the  case  of  the  liver  may  have  discouraged  clinicians 
from  studying  it,  and  helps  to  account  for  the  neglect  which 
has  been  so  marked  in  the  past  in  connection  with  this 
branch  of  clinical  observation. 

Percussion  of  the  heart  in  the  adolescent  type  of 
dilatation  of  the  right  ventricle. — The  increase  in  the  size  of 
the  right  ventricle  upwards  and  to  the  left,  which  charac- 
terises this  type  of  dilatation,  will  naturally  lead  to  an  in- 
crease in  the  amount  of  cardiac  dullness  in  this  direction — 
namely,  an  increase  in  the  normal  amount  of  dullness  in 
the  third  interspace  and  the  appearance  of  abnormal  cardiac 
dullness,  first  relative  and  later  absolute,  in  the  second 
interspace.  In  extreme  cases  there  may  be  absolute  cardiac 
dullness  for  2  inches  or  more  in  the  second  left  interspace 
and  to  a  corresponding  extent  in  the  third,  and  the  rela- 
tive dullness  may  even  reach  up  into  the  first  interspace. 
Increase  of  the  cardiac  dullness  of  this  type  is  not  as  a  rule 
accompanied  by  any  increase  to  the  right,  and  in  these 
cases  the  sternum  is  usually  resonant  do^vn  to  the  level  of  the 
fourth  interspace  or  fifth  rib.  This  resonance  of  the  sternum 
does  not  mean  that  the  heart  is  not  in  close  contact  with  it 
till  such  a  low  level  is  reached,  for  the  sternum  being  a  single 
flat  bone  takes  the  note  of  that  structure  with  which  it  is 
mostly  in  contact.  If  the  lung  be  in  contact  with  its  under- 
surface  for  more  than  half  its  length  the  note  it  gives  is 
mainly  resonant  ;  if  the  heart,  on  the  other  hand,  be 
so  enlarged  as  to  displace  the  lung  for  more  than  half  its 
length  the  sternum  will  be  mainly  dull.  This  fact  accounts 
for  the  sudden  changes  in  the  size  of  the  area  of  the  cardiac 


26  ADOLESCENT  TYPE  OF  DILATATION 

dullness  which  may  sometimes  be  noted  when  a  heart  which 
has  been  occupying  rather  less  than  half  the  length  of  the 
sternum  increases  a  little  in  size  so  as  to  occupy  rather  more 
than  half,  or  vice  versa. 

The  absence  of  dilatation  to  the  right  of  the  sternum  has 
already  been  referred  to,  and  is  well  shown  in  fig.  99,  p.  288. 

In  well-marked  cases  of  dilatation  of  the  conus  arteriosus 
the  outline  of  the  heart  varies  considerably,  and  its  general 
characteristics  are  sufficiently  well  shown  in  figs.  68-75,  and  do 
not  call  for  further  description  here,  where  we  are  dealing  with 
early  diagnosis  only.  The  fact  of  an  increase  in  the  amount 
of  dullness  in  the  recumbent  position  as  compared  with  the 
amount  when  the  patient  is  erect  is  also  dwelt  upon,  and  the 
reasons  for  this  change,  given  in  the  Essay  on  the  Condition 
of  the  Heart  in  Anaemia. 

Auscultation  of  the  Heart  in  Adolescent  Dilatation  of 
the  Eight  Ventricle. — Auscultation  caimot  always  be  relied 
upon  as  a  means  of  diagnosing  adolescent  dilatation  of  the 
right  ventricle,  because  auscultatory  signs  may  be  absent 
even  in  well-marked  cases  ;  they  are  as  a  rule,  however,  both 
definite  and  characteristic. 

The  chief  sign  of  this  upward  dilatation  is  the  occurrence 
of  a  systolic  murmur  in  the  pulmonary  artery.  The  clinical 
and  pathological  discussion  of  this  murmur  will  be  found  at 
pp.  247-253  and  p.  254,  and  it  is  there  shown  that  the  features 
of  this  murmur  are  as  follows  : — 

It  is  produced  in  the  pulmonary  artery  under  the  following 
circumstances.  Owing  to  the  upward  extension  of  the  anterior 
wall  of  the  right  ventricle  the  level  of  the  pulmonary  valves 
is  raised,  and  therefore  the  point  of  origin  of  the  pulmonary 
artery  is  brought  nearer  to  its  termination,  which  is  a  fixed 
point.  There  must,  therefore,  be  some  degree  of  relaxation 
of  its  elastic  walls,  and  when  the  blood  pressure  rises  during 
systole  this  relaxation  will  result  in  the  development  of  an 
anemysm-like  dilatation  of  the  artery.  In  this  a  murmur  is 
produced  just  as  is  the  case  in  an  ordinary  aneurysm.  The 
main  factors,  therefore,  wdiich  are  concerned  in  the  production 
of  the  murmur  are  :  firstly,  the  relaxation  of  the  elastic  wall 
of  the  pulmonary  artery ;  secondly,  a  blood  pressure  adequate 


PULMONARY  ARTERY  MURMUR  27 

for  its  over-distension ;  and  thirdly,  a  pulmonary  orifice 
sufficiently  small  in  comparison  with  the  dilated  artery  to 
admit  of  the  fonnation  of  mumiur-producing  eddies  in  it. 

The  greater  the  relaxation  the  louder  therefore  will  be  the 
murmur,  if  the  other  factors  are  equal.  Where  there  is  more 
lateral  dilatation  of  the  ventricle  and  less  upward  dilatation 
a  less  loud  murmur  will  be  heard  than  where  the  dilatation 
is  mainly  upward.  Also,  in  the  erect  posture  the  weight  of 
the  heart  tightens  the  artery  more  than  is  the  case  when  the 
patient  is  recumbent,  therefore  the  murmur  is,  as  a  rule,  less 
loud  in  the  erect  position. 

From  what  has  just  been  said  it  will  be  seen  that  the  essential 
point  in  the  production  of  the  murmur  is  the  distension  of 
the  artery  so  that  the  diameter  of  its  lumen  exceeds  that  of 
the  pulmonary  orifice.  Were  the  pulmonary  orifice  itself  to 
be  dilated  to  nearly  the  same  extent  as  the  artery,  no  murmur 
would  be  produced  by  the  inrush  of  blood  into  the  dilated 
artery.  In  many  cases  of  extreme  upward  dilatation — when, 
for  instance,  the  pulmonary  valves  are  at  the  level  of  the  upper 
border  of  the  first  rib  or  higher — it  is  found  that  a  pulmonary 
murmur  is  not  present,  or  if  present  is  only  very  faint,  and  the 
reason  is  almost  certainly  that  just  stated — namely,  that 
the  pulmonary  orifice  is  dilated  as  well  as  the  pulmonary 
artery. 

Also,  for  the  production  of  the  murmur  there  must  be 
sufficient  distending  force.  The  amount  of  distension  will 
be  proportional  to  the  excess  of  the  internal  pressure  in  the 
artery  over  the  external  resistance.  Therefore,  when  the  heart 
is  weak  a  comparative  feebleness,  or  even  an  absence  of  murmur, 
may  be  observable  in  spite  of  considerable  dilatation  of  the 
ventricle.  In  such  a  case  the  mm-mur  will  be  found  to  appear 
as  the  heart  gains  in  strength  {vide  p.  305).  To  take  the 
opposite  extreme,  a  very  loud  murmm*  usually  occurs  in 
anaemia  because  there  is,  in  this  condition,  a  marked  rise  in 
the  blood  pressure  in  the  pulmonary  artery  (as  shown  by  the 
loud  second  sound,  vide  p.  244)  as  well  as  upward  dilatation  of 
the  ventricle. 

It  is  possible  also  that  increased  support  to  the  artery, 
from  consolidation  of  the  adjacent  lung  or  other  cause,  would 


28  ADOLESCENT  TYPE  OF  DILATATION 

diminish  tho  loudness  of  the  murmur  by  Hmiting  the  amount 
of  dilatation. 

To  sum  up :  a  loud  murmur  is  to  be  expected  in  cases 
of  absolute  overstrain  unless  the  pulmonary  orifice  be  dilated 
as  well  as  the  artery,  or  unless  there  be  sufficient  resistance 
from  adjacent  structures  to  prevent  the  over-distension  of  the 
artery  :  and  a  faint  or  absent  murmur  is  to  be  expected  in 
cases  of  relative  overstrain  where  the  ventricular  dilatation, 
is  due  to  weakened  ventricular  walls,  coupled  as  this  must 
be  with  a  lowered  blood  pressure  in  the  pulmonary  artery 
as  a  result  of  the  muscular  weakness.  The  clinical  character- 
istics of  this  murmur  are  dealt  with  in  detail  at  pp.  254-277, 
and  its  differential  diagnosis  at  p.  215. 

From  what  has  just  been  said  it  will  be  seen  that  accentua- 
tion of  the  pulmonary  second  sound  and  increased  loudness 
of  the  right  ventricular  first  sound  are  merely  signs  of  absolute 
overstrain  of  the  right  ventricle,  and,  while  usually  accompanying 
this  type  of  dilatation,  cannot  be  considered  characteristic 
of  it. 

For  a  fuller  discussion  of  the  clinical  features  of  the 
adolescent  type  of  heart  failure  the  reader  is  referred  to  the 
Essay  on  the  Condition  of  the  Heart  in  Anaemia,  at  p.  227. 

How  TO  Detect  the  First  Signs  of  Cardiac  Failure 

Having  now  outlined  the  various  symptoms  and  signs  to 
which  this  type  of  cardiac  dilatation  gives  rise,  we  are  in  a  position 
to  point  out  their  practical  application  in  answer  to  the  ques- 
tion :  '  How  shall  I  detect  the  first  signs  of  cardiac  failure  in  a 
patient  ?  ' 

Suppose  it  is  a  question  whether  an  adolescent  is  overtaxing 
the  heart  by  physical  exertion  of  some  sort,  or  whether  a 
person  who  has  had  rheumatic  fever  is  beginning  to  walk 
about  before  being  really  well  enough  to  do  so  ;  or  perhaps 
the  question  is  whether  a  young  woman  suffering  from  anaemia 
had  better  take  an  active  or  a  passive  holiday.  The  answer 
depends  upon  the  question  :  '  Is  the  right  ventricle  begiiming 
to  fail  or  not  ?  ' 

The   first   sign  of   failure   is   breathlessness   on   exertion ; 


EARLY  DIAGNOSIS  29 

but  this  may  not  be  present  to  a  sufficient  extent  to  be 
diagnostic.  The  pulse,  too,  may  show  httle,  if  any,  departure 
from  the  normal.  We  shall  therefore  have  to  turn  to  the 
examination  of  the  heart. 

1.  The  first  unequivocal  sign  for  which  we  look  in  such  a 
case  is  an  increase  in  the  amount  of  the  cardiac  pulsation 
over  the  body  of  the  right  ventricle — ^i.e.,  over  the  fourth 
left  interspace  between  the  nipple  hne  and  the  sternum.  This 
shows  commencing  overaction  of  the  right  ventricle  and 
■will,  if  the  case  be  one  of  absolute  overstrain,  be  accompanied 
by  some  increase  in  the  true  loudness  of  the  pulmonary  second 
sound.  A  slight  increase  in  the  loudness  of  the  first  sound, 
as  heard  over  the  right  ventricle,  may  also  be  noticeable  if 
the  case  has  been  under  careful  observation  previously. 

In  cases  of  relative  overstrain — such  as  in  a  heart  weakened 
by  rheumatic  fever — there  may,  or  may  not,  be  this  increase 
in  the  loudness  of  the  sounds.  If  the  failure  be  primarily 
of  the  left  ventricle  and  the  right  ventricular  failure  be 
secondary  to  this,  an  increased  loudness  of  the  sounds  will 
be  noticeable.  If,  on  the  other  hand,  the  main  cause  of  the 
increased  pulsation  be  the  undue  distensibihty  of  the  right 
ventricle  itself,  there  will  be  no  increase  in  the  loudness  of  the 
sounds  it  is  producing. 

In  addition  to  the  signs  mentioned  there  will  be  some 
fullness  of  the  neck  veins — probably  with  some  amount  of 
false  pulsation  in  them. 

2.  If  the  heart  have  reached  a  somewhat  more  advanced 
stage  of  failure,  we  shall  find  evidence  that  the  weakest  part 
of  the  wall  of  the  right  ventricle  cannot  withstand  the  intra- 
ventricular pressm-e  and  is  beginning  definitely  to  dilate. 

In  the  distensible  hearts  of  which  we  are  speaking,  this 
weakest  part  is  the  so-called  conus  arteriosus  of  the  right 
ventricle  ;  this — the  weakest  part  of  the  ventricle — being 
dilated  by  the  action  of  the  stronger  part. 

These  signs  are  increase  of  the  cardiac  dullness  and  the 
appearance  of  cardiac  pulsation  in  the  third  left  interspace. 

3.  The  next  series  of  phenomena  are  due  to  the  further 
dilatation  of  the  right  ventricle  upward. 

They  consist  in  the   appearance  of  cardiac  dullness,  first 


30  ADOLESCENT  TYPE  OF  DILATATION 

relative  and  then  absolute,  in  the  second  left  interspace  and, 
linally,  of  cardiac  pulsation  in  this  situation.  Accompanying 
this  dilatation  there  will  be  (where  the  overstrain  of  the  right 
ventricle  is  absolute,  not  relative)  the  appearance  of  a  pul- 
monary systolic  murmur,  together  with  increasing  loudness 
of  the  pulmonary  second  sound  and  of  the  right  ventricular 
first  sound. 

There  will  also  be  more  marked  fullness  of  the  veins  of 
the  neck. 

These  phenomena  may  become  extremely  well  marked 
in  cases  of  ansemia,  so  much  so  that  there  may  be  dullness 
and  pulsation  for  two  inches  or  more  in  the  second  left  inter- 
space and  the  murmur  may  be  so  loud  as  to  be  conducted 
into  the  arteries  of  the  neck  (omng  to  the  physical  contact 
between  the  arch  of  the  aorta  and  the  pulmonary  artery),  and 
may  also  be  accompanied  by  a  vibratile  thrill  which  is  distinctly 
palpable  in  the  second  left  interspace  over  the  site  of  the 
pulmonary  artery,  and  which  is  more  marked  when  the 
patient  is  recumbent  than  when  erect. 

4.  The  next  group  of  phenomena  that  would  appear  in  a 
failing  right  ventricle  are  the  phenomena  wliich  indicate  that 
the  main  body  of  the  right  ventricle  is  giving  way  in  the 
face  of  the  extra  blood  pressure  which  it  is  called  upon  to 
develop.  Tliis  gi'oup  of  phenomena  does  not  occur,  as  a 
rule,  in  cases  of  relative  overstrain,  but  only  where  the  ventricle 
may  be  expected  to  be  maintaining  a  blood  pressure  higher 
than  normal. 

This  general  dilatation  of  the  right  ventricle  is  associated 
with  increase  of  the  heart  to  the  right — the  well-known  and 
usually  described  type  of  right  ventricular  dilatation.  As  has 
already  been  pointed  out,  tliis  type  of  dilatation  is  more 
characteristic  of  the  moderately  distensible  heart  of  adult  hfe 
than  of  the  distensible  heart  of  adolescence,  and  its  occurrence 
under  the  latter  conditions  would  imply  a  very  extreme  degi'ee 
of  cardiac  failure  such  as  would  occur  in  severe  valvular  disease. 

The  subject  of  dilatation  of  the  ventricle  to  the  right  and  the 
symptoms  associated  with  it  are  dealt  with  later  on  when 
discussing  cardiac  failure  in  hearts  of  moderate  distensiblity,  and 
so  no  more  need  be  said  here  on  the  subject. 


ADULT  TYPE  OF  DILATATION  31 

Early  Diagnosis  of  Heart  Failure  with  Enlargement 
IN  Hearts  of  Moderate  Distensibility 

We  have  now  to  take  up  the  early  diagnosis  of  heart  failure 
in  a  moderately  distensible  heart,  such  as  that  usually  found 
in  early  adult  and  middle  hfe.  The  way  in  which  the  early 
signs  differ  from  those  seen  in  adolescence  has  already  been 
outUned,  and  it  has  been  pointed  out  that  this  difference  appears 
to  be  due  to  the  fact  that  the  fibrous  elements  of  the  heart 
and  pericardium,  being  newly  formed  and  distensible  in 
adolescence,  are  not  able  to  exert  much  influence  in  checking 
over-distension  of  the  organ  ;  whereas  in  maturity  and  later 
life  the  restraining  power  of  the  fibrous  tissues  increases. 

The  main  consequence  of  the  increased  strength  of  the 
fibrous  elements  is  that  the  heart  no  longer  has  to  depend 
mainly  upon  its  muscular  tissue  for  the  prevention  of  over- 
distension and  therefore  the  shght  local  variations  in  the 
muscular  strength  of  its  wall  do  not,  in  later  life,  determine 
the  part  which  will  be  the  first  to  yield  to  undue  strain,  as 
was  the  case  m  adolescence. 

When  the  heart  is  depending  mainly  upon  its  fibrous 
tissues  for  the  prevention  of  over-distension,  the  following 
points  are  noticeable. 

In  overstrain  involving  both  sides  of  the  heart — such  as 
that  from  over-exertion,  cycling,  climbing,  &c.— there  is  not 
a  great  disparity  in  the  dilatabihty  of  the  two  sides,  and 
we  therefore  expect  to  find  dilatation  of  both  the  right  and 
left  ventricles. 

Moreover,  there  is  not  the  same  differential  yieldmg  of  the 
wall  of  the  right  ventricle  that  occurs  in  adolescence,  but  both 
the  right  and  the  left  ventricle  ddate  in  a  very  similar  manner 
in  the  face  of  an  excessive  resistance  to  the  outflow  of  blood 
dming  systole. 

If  the  wall  of  the  left  ventricle  be  looked  at,  it  vn\l  be  seen 
that  there  is  a  decided  difference  between  its  thickness  at  the 
apex  and  round  the  base  near  the  amiculo-ventricular  orifice. 
If  the  relative  thickness  of  the  walls  during  ventricular  systole 
be  considered,  it  will  be  recognised  that  this  difference  will 
be  accentuated.    Now,  suppose  that  the  ventricle  is  working 


32  ADULT  TYPE  OF  DILATATION 

against  an  arterial  resistance  of  increasing  magnitude.  A  point 
can  be  reached  where  the  resistance  to  be  overcome  requires 
a  rise  in  the  intraventricular  pressure  which  is  in  excess  of 
the  resisting  power  of  the  thinner  basal  part  of  the  wall,  but 
is  not  too  great  for  the  expulsive  power  of  the  stronger  apical 
part.  Li  meeting  such  a  resistance  as  this  there  will  be 
a  shght  stretching  of  the  weaker  part  of  the  wall  with  each 
recurring  systole.  The  stronger  apical  part  will  in  this  way- 
dilate  the  weaker  basal  part.  The  fact  that  this  basal  portion 
is  the  last  to  be  emptied  also  involves  a  more  prolonged  strain 
upon  it  than  upon  the  apical  portions  of  the  ventricle. 

The  over- distension  of  the  basal  portion  involves  another 
important  change,  and  that  is  the  over-stretching  of  the  muscular 
and  fibrous  ring  of  the  mitral  valve.  Stretching  of  the  fibres 
of  this  ring  will  tend  to  the  enlargement  of  the  orifice  and  to 
mitral  regurgitation.  This,  as  is  well  known,  is  of  the  nature 
of  a  safety  valve  action,  for  the  escape  of  blood  into  the 
auricle  will  lower  the  intraventricular  pressure  at  the  time 
of  maximal  strain  and  so  lessen  the  tendency  to  further 
dilatation.  Were  it  not  for  this,  a  dilatation  of  the  ventricle 
once  begun  would,  theoretically,  continue  unchecked  until 
enormous  distension  resulted. 

In  the  case  of  the  right  ventricle,  the  same  sequence  of 
phenomena  will  take  place.  The  weaker  basal  portion  being 
dilated  by  the  stronger  apical  part  and  the  dilatation  being 
arrested  by  the  production  of  incompetence  of  the  tricuspid 
valve. 

In  adult  life  we  often  see  well-marked  dilatation  of  this 
basal  portion  of  the  right  ventricle  without  any  differential 
yielding  of  the  shghtly  thinner  part  of  the  wall  near  the 
pulmonary  valves. 

Where  this  occm'S,  we  are,  I  think,  justified  in  saying  that 
the  fibrous  tissues  of  the  heart  are  taking  the  major  part  in 
preventing  dilatation  of  the  ventricle. 

This  type  of  dilatation  may  well  be  called  the  adult  type 
of  dilatation  as  distinct  from  the  adolescent  type  aheady 
dealt  with.  As  has  already  been  pointed  out,  it  is  not  intended 
to  imply  that  in  an  adult  this  type  of  dilatation  Avill  always 
be  found,  because  some  degree  of  the  adolescent  distensibihty 


CARDIAC  DISTENSIBILITY  IN  ADULT  LIFE  33 

of  the  heart  may  be  retained  in  adult  Life.  If  these  two  types 
of  dilatation  are  recognised,  however,  the  distensibility  of 
any  particular  heart  can  be  judged  by  the  degree  in  which  it 
conforms  to  one  or  other  of  these  types. 

For  instance,  a  heart  showing  slight  dilatation  of  the  conus 
arteriosus  of  the  right  ventricle  and  well-marked  dilatation  of 
the  body  of  the  ventricle  must  be  taken  as  having  nearly  lost 
its  adolescent  distensibility.  A  heart  with  proportionally 
more  dilatation  of  the  thin  part  of  the  muscular  wall  must  be 
a  heart  whose  fibrous  tissues  are  less  rigid,  and  a  heart  showing 
less  upward  dilatation,  in  spite  of  well-marked  dilatation 
to  the  right,  must  be  a  heart  whose  fibrous  tissues  have  more 
resisting  power. 

The  relative  amount,  therefore,  to  which  one  or  other 
or  both  of  these  two  types  of  dilatation  is  present  (in  any 
particular  case  of  heart  failure)  gives  important  information 
as  to  the  condition  of  the  heart  so  far  as  the  strength  or 
otherwise  of  its  fibrous  elements  is  concerned. 

In  dealing  with  the  early  diagnosis  of  heart  failure  in  hearts 
of  moderate  distensibility  what  has  just  been  spoken  of  as 
the  adult  type  of  dilatation  only  will  be  considered,  and  the 
physical  signs  will  be  described  which  occur  when  the  fibrous 
tissues  are  sufficiently  resistant  to  prevent  the  adolescent 
type  of  dilatation  from  occurring  at  all. 

Before,  however,  taking  up  the  subject  in  detail  it  will 
be  well  to  discuss  shortly  the  distensibility  of  the  heart  in 
its  bearing  upon  heart  failure  with  dilatation  in  adult  life. 

Distensibility  of  the  Heart  in  Adult  Life 

Although  the  age  of  the  patient  has  been  mentioned  as 
roughly  determining  the  amount  of  distensibility  possessed  by 
the  heart,  it  cannot  be  so  used  in  any  absolute  sense,  for  the 
distensibility  in  a  series  of  patients  of  any  particular  age  may 
vary  considerably.  In  some  patients  the  rigidity  of  the  fibrous 
tissues  of  the  heart  appears  to  be  much  more  marked  than  in 
others.  Patients  of  seventy  or  eighty  may  be  met  with  in 
whom  the  heart  appears  to  be  still  quite  distensible.  For 
instance,  I  have  known  an  old  lady  of  over  eighty  live  for 


34  ADULT  TYPE  OF  DILATATION 

years  with  a  heart  so  large  that  its  pulsation  could  be  felt  over 
the  whole  chest  from  the  right  nipple  line  up  to  the  left  axilla 
{vide,  p.  320).  On  the  other  hand,  patients  of  under  fifty- 
may  show  evidences  of  well-marked  absence  of  distensibihty. 

When  dealing  with  heart  failure  in  adult  life  it  is  important 
to  estimate  the  degree  of  rigidity  which  is  present,  because 
the  management  of  the  patients — the  medicinal  treatment 
and  the  prognosis — depend  upon  the  distensibihty  of  the  heart. 

This  additional  factor  of  fibrous  rigidity  complicates  the 
question  of  heart  failure.  In  adolescence  the  problem  was 
a  simple  one,  because  there  were  only  two  points  to  consider — 
namely,  the  strength  of  the  muscular  wall  and  the  resistance 
to  the  circulation  which  the  heart  had  to  overcome  ;  therefore 
the  amount  of  dilatation  occurring  was  easily  to  be  understood 
and  interpreted  by  the  study  of  these  two  factors. 

The  problem  we  have  now  to  deal  with  is  not  so  easy. 
For  instance,  suppose  two  hearts  of  equal  muscular  strength 
and  working  against  the  same  circulatory  resistance,  but  in  the 
one  case  the  fibrous  tissues  are  more  resistant  than  in  the  other. 

The  one  with  the  less  resistant  fibrous  tissues  will  dilate 
more  than  the  other  one  will ;  yet  it  does  not  follow  that 
the  heart  which  does  not  dilate  is  the  better  organ  of  the  two. 
Therefore,  in  dealing  with  a  heart  in  adult  and  later  life,  we 
have  before  us,  as  it  were,  an  equation  with  three  quantities, 
two  of  which  are  unknown,  and  which  we  therefore  carmot 
solve  ;  instead  of  the  equation  with  two  quantities,  one  of 
which  is  known,  which  is  presented  to  us  by  the  adolescent 
heart. 

As  is  the  case  with  algebra,  we  must  try  to  find  a  second 
equation  whereby  two,out  of  our  three  unknown  quantities  may 
become  known,  and  we  fortunately  can  often  succeed  in  esti- 
mating approximately  two  out  of  the  three  factors  concerned 
— namely  : — 

1.  Muscular  strength  of  heart  wall. 

2.  Degree  of  fibrous  rigidity  of  the  heart  wall  (that  is, 
its  distensibihty). 

3.  The  resistance  against  which  the  heart  is  working. 
Therefore,  when    considering   the    early  signs   of   cardiac 

failure  in  middle  and  later  life,  we  cannot  rely  upon  the  amount 


EAKLY  SIGNS  35 

of  dilatation  as  a  trustworthy  guide  to  the  degree  of  failure 
present  as  was  the  case  in  early  life.  We  have  to  be  on  the 
look  out  for  other  signs  of  cardiac  failure  before  we  can  appraise 
at  its  true  value  the  presence  or  absence  of  enlargement  of 
the  heart  in  any  particular  case.  This  subject  will,  however, 
be  further  discussed  when  speaking  of  heart  failure  without 
enlargement,  and  the  points  raised  will  be  better  dealt  with 
there  than  here. 

At  present,  we  shall  simply  deal  with  phenomena  observable 
where  a  heart  of  moderate  distensibility  fails,  and  leave  the 
question  how  best  to  recognise  the  degree  of  distensibility 
possessed  by  the  heart  until  the  question  of  heart  failure  without 
enlargement  is  discussed. 

Early  Signs  of  Failure  with  Enlargement  in  Hearts 
OF  Moderate  Distensibility 

Changes  in  the  Pulse. — The  first  evidences  of  heart 
failure  here,  as  in  more  distensible  hearts,  are  to  be  found  in 
the  pulse,  if  the  patient  have  been  under  observation  before 
the  heart  failure  set  in  and  the  normal  character  of  the  pulse 
be  known.  Under  other  circumstances,  the  pulse  is  a  less 
certain  guide  in  middle  and  later  life  than  it  was  in  early  hfe, 
because  of  its  character  depending  in  part  upon  the  condition 
of  the  arteries  and  not  wholly  upon  the  strength  of  the  heart, 
One  instance  will  suffice  to  illustrate  the  uncertainty  which 
changes  in  the  arterial  wall  or  in  the  blood  pressure  bring  about. 

Take  the  case  of  a  patient  between  fifty  and  sixty  suffering 
from  a  severe  attack  of,  say,  abdominal  pain,  in  whose  case 
the  question  arises  :  Is  there  any  temporary  weakening  of 
the  heart  ?  On  examining  the  pulse  it  was  found  that  the 
arterial  walls  were  fairly  soft  and  approximately  normal,  as 
judged  by  the  finger,  and  that  the  pulse  was  regular  and  of 
fair  volume  and  strength  and  of  moderate  tension. 

Judging,  therefore,  by  the  condition  of  the  pulse  there  was 
no  marked  weakening  of  the  heart.  When,  however,  the  pain 
had  passed  off  in  a  few  hours'  time,  it  was  found  that  the 
man's  usual  pulse  was  very  full  and  of  high  tension,  and  that 
during  the  attack  of  pain  there  had  been  a  very  considerable 

d2 


36  ADULT  TYPE  OF  DILATATION 

amount  of  temporary  heart  weakness.  Had  this  man  been  first 
seen  dming  a  severe  attack  of  influenza,  or  other  condition 
accompanied  by  toxaemic  affection  of  the  heart  muscle,  an 
estimate  of  the  presence  or  absence  of  heart  weakness,  based 
mainly  on  the  pulse,  might  have  led  to  a  disastrous  error 
in  diagnosis. 

Therefore  the  pulse  must  be  used  vdih  caution  as  a  guide 
in  diagnosing  the  absence  of  heart  failure  in  middle  life.  The 
further  discussion  of  the  indications  given  by  the  pulse 
will  be  postponed  till  the  question  of  heart  failure  without 
enlargement  is  taken  up  {vide  p.  59). 

Dyspncea. — In  this,  as  in  other  types  of  cardiac  failure, 
breathlessness  on  exertion  is  one  of  the  earhest  and  most 
important  symptoms,  but  its  characteristics  are  so  well  known 
that  little  need  be  said  upon  the  subject  here. 

In  the  moderately  distensible  heart  of  middle  life  breath- 
lessness  is  less  often  associated  with  sighing  breathing  than 
is  the  case  in  adolescence  ;  and  although  the  patient  with 
dyspnoea  can  sometimes  get  reUef  from  taking  a  long  sighing 
breath,  this  type  of  breathing  is  not  so  well  marked  a  phenomenon 
as  it  is  in  early  life. 

The  diagnostic  value  of  dyspna  a  on  exertion  is  somewhat 
lessened  in  middle  hfe  by  the  fact  that  it  is  more  apt  than  in 
early  life  to  be  due  to  causes  other  than  actual  heart  failure 
{vide  p.  113). 

On  the  other  hand,  in  middle  hfe,  dyspnoea  on  exertion 
when  certainly  due  to  cardiac  failure  is  of  graver  significance 
than  it  is  in  adolescence.  This  is  due  to  the  fact  already 
pointed  out  that  in  the  moderately  distensible  heart  there 
is  less  disparity  in  the  dilatability  of  the  two  sides  of  the  heart 
than  in  the  distensible  one,  and  therefore,  whereas  in  the  dis- 
tensible heart  of  adolescence  dyspnoea  can  be  caused  by  an 
amount  of  embarrassment  which  is  too  slight  to  interfere 
with  the  stronger  left  ventricle,  in  later  hfe  this  is  not  the 
case,  and  dyspnoea  is  not  hkely  to  occur  until  the  strain  is 
great  enough  to  interfere  ■with  the  left  ventricle  as  well  as 
with  the  right. 

Pain. — Cardiac  pain  is  a  far  commoner  symptom  of  heart 


EARLY  SIGNS  37 

failure  in  middle  and  later  life  than  it  is  in  early  life,  but  ae 
it  is  especially  characteristic  of  cases  where  cardiac  failure 
occurs  in  relatively  rigid  hearts,  its  discussion  will  be  post- 
poned until  tliis  subject  is  dealt  with  {vide  p.  82). 

Another  type  of  pain  which  gives  important  evidence 
of  heart  failure  is  that  which  occurs  over  the  liver  and  is  duo 
to  over-distension  of  the  hepatic  vein  in  tricuspid  regui'gita- 
tion  ;  but  it  is  a  late  rather  than  an  early  sign,  except  in  the 
case  of  chronic  heart  failure,  such  as  that  due  to  valvular 
disease — where  the  sudden  onset  of  pain  over  the  Uver 
may  be  an  early  sign  that  compensation  is  beginning  to 
give  way. 

The  general  symptoms  of  dropsy  and  cyanosis  occur  as 
late  rather  than  early  signs  of  cardiac  failure,  and  there  is 
nothing  of  special  importance  to  be  noted  about  them  in 
connection  with  the  present  subject. 

Physical  Signs  of  cardiac  failure  in  hearts  of  moderate 
distensibility. — As  has  been  already  pointed  out,  the  distinctive 
change  in  moderately  distensible  hearts,  so  far  as  the  right 
ventricle  is  concerned,  is  a  general  yielding  and  distension 
of  the  wall  around  the  tricuspid  valve,  causing  a  broadening 
of  the  heart  towards  the  right,  and  also  leading  to  systolic 
regurgitation  of  blood  through  the  tricuspid  valve. 

The  main  clinical  features  of  which  we  have  now  to  speak 
result  from  these  two  phenomena. 

Firstly,  as  regards  the  tricuspid  regurgitation.  The 
way  in  wliich  tricuspid  incompetence  arises  and  its  relationship 
to  dilatation  of  the  right  ventricle  have  already  been  referred  to. 
The  phenomena  due  to  the  regurgitation  of  blood  during  the 
ventricular  systole  must  now  be  studied.  The  simple  state- 
ment that  the  regurgitating  blood  enters  the  right  auricle 
and  causes  its  ultimate  dilatation  and  then  causes  a  systolic 
distension  of  the  veins — while  summarising  what  often  happens 
— does  not  express  sufficiently  accurately  what,  in  all  probabihty, 
takes  place.  The  old  view  used  to  be  that,  after  its  contraction, 
the  auricle  was  in  a  state  of  relaxation,  and  was  therefore  the 
unresisting  recipient  of  any  blood  that  was  incHned  to  enter 


38  ADULT  TYPE  OF  DILATATION 

it.  If  this  were  the  case  the  statement  just  made  would  be 
ample  and  accurate. 

There  is,  however,  good  reason  to  believe  that  the  auricular 
wall  possesses  a  certain  amount  of  tonic  activity,  even  during 
its  diastole,  and  there  is  little  doubt  that  the  walls  of  the 
veins,  too,  possess  a  large  measure  of  tonic  contractile  power. 

If  tliis  be  so,  the  question  as  to  the  course  taken  by  the 
blood  when  it  regurgitates  through  the  tricuspid  valve  may 
not  be  such  a  simple  one,  and  may  be  stated  as  follows  : — 

If  the  tone  of  the  auricular  wall  be  good  it  may  be  possible 
for  it  to  resist  the  sudden  distension  of  the  auricle  by  the  blood 
which  regurgitates  through  the  tricuspid  valve  and  so  to  deflect 
the  stream  of  blood  into  the  veins,  causing  their  dilatation. 

If,  on  the  other  hand,  the  muscular  tone  of  the  veins  is 
better  than  that  of  the  auricle  the  latter  would  be  distended 
rather  than  the  former. 

But  in  speaking  of  the  veins  entering  the  auricle,  we  are 
speaking  of  the  inferior  as  well  as  the  superior  cava,  and  the 
above  statement  must  in  consequence  be  amplified  thus  : — 

When,  owing  to  the  better  muscular  tone  of  the  right 
auricle  or  to  the  excessive  amount  of  the  tricuspid  incom- 
petence, the  regurgitating  blood  tends  to  dilate  the  veins,  it  may 
pass  either  upwards  into  the  superior  cava  or  downwards  into 
the  inferior  cava,  or  in  both  directions  simultaneously.  Now, 
clinically,  it  would  appear  that  the  Eustachian  valve  (with 
or  without  the  assistance  of  the  valves  of  the  inferior  vena 
cava  and  the  muscularity  of  the  vein)  is  able  to  offer  more 
resistance  to  the  downward  passage  of  the  regurgitating  blood 
than  can  be  offered  by  the  tonic  contraction  of  the  superior 
cava  (aided  by  the  subclavian  and  other  valves)  to  its  upward 
passage,  and  that  therefore  it  is  more  frequent  for  tricuspid  regur- 
gitation in  its  earlier  stages  to  cause  distension  of  the  superior 
cava  and  its  branches  than  of  the  inferior  cava  and  hver. 

Nevertheless,  it  is  not  very  unusual  to  find  that  venous 
engorgement  of  the  liver  is  present  in  the  absence  of  any 
marked  reflux  into  the  superior  cava,  and  therefore  absence 
of  tricuspid  regurgitation  cannot  be  diagnosed  until  the  state 
of  the  liver  has  been  carefully  noted. 

False  Venous  Pulsation. — With  regard   to  the  clinical 


VENOUS  PHENOMENA  39 

phenomena  of  venous  plethora  due  to  tricuspid  regurgitation, 
what  has  already  been  said  as  to  false  pulsation  in  the 
veins  holds  good  also  for  the  earlier  stages  of  venous  plethora 
in  hearts  of  only  moderate  distensibility  where  tricuspid 
regurgitation  is  commencing. 

In  some  cases  of  sudden  failure  of  the  right  ventricle,  as 
from  a  severe  asthmatic  seizure,  extreme  venous  engorgement 
may  be  seen  with  well-marked  false  pulsation,  but  with  no 
sign  of  true  systolic  pulsation. 

As  this  subject  has  been  dealt  with  at  p.  14,  and  will 
be  again  referred  to  at  p.  137,  more  need  not  be  said  here, 
except  to  point  out  that  the  feebler  the  muscular  tone  of 
the  over-distended  veins  the  more  marked  will  be  the  false 
pulsation  which  is  observable. 

True  Systolic  Pulsation  in  the  Veins. — When  the 
pulsatile  movements  in  the  over-distended  veins  of  the  neck 
are  carefully  watched  and  timed  by  listening  to  the  heart  sounds 
or  palpating  the  cardiac  impulse,  it  is  quite  easy  to  distinguish 
true  from  false  pulsation  and  to  note  the  characteristic  systolic 
filling  of  the  veins  from  below  upward. 

In  the  slighter  cases  before  the  giving  way  of  the  subclavian 
and  innominate  valves  it  is  necessary  to  note  carefully  the 
movements  of  the  so-called  jugular  bulb  at  the  root  of  the 
jugular  vein,  and  of  the  innominate  vein  so  far  as  it  is  palpable 
or  visible  in  the  episternal  notch. 

When  the  tricuspid  regurgitation  is  more  copious  a  well- 
marked  systolic  filling  of  the  jugular  and  other  veins  of  the 
neck  will  be  noticeable. 

When  the  tricuspid  regurgitation  is  very  extreme,  and  the 
muscular  tone  of  the  veins  is  good,  their  tenseness  and  the 
vigour  of  their  pulsation  may  lead  to  their  being  mistaken 
for  pulsating  arteries  and  give  rise  to  an  error  in  diagnosis  on 
the  part  of  a  superficial  observer  {vide  pp.  87  and  222). 

Enlargement  of  the  Liver. — Another  well-known  and 
important  sign  of  failure  of  the  right  ventricle  is  enlargement 
of  the  Hver,  due  to  tricuspid  regurgitation  downwards  into 
the  hepatic  vein.  This  is,  however,  a  late  rather  than  an  early 
sign  of  cardiac  failure,  and  need  not  be  further  referred  to  in 
connection  with  the  present  subject. 


40  ADULT  TYPE  OF  DILATATION 

Physical  Signs  ov  Dilatation  of  the  Eight  Ventricle, 
— As  was  the  case  in  distensible  hearts,  the  first  sign  that  the 
right  ventricle  is  having  an  abnormal  amount  of  work  to  do 
'  is  to  be  found  in  an  increase  of  the  cardiac  impulse  in  the 
fourth  left  interspace  over  the  body  of  the  ventricle.  An 
increase  of  cardiac  pulsation  here  often  gives  the  first  sign 
of  cardiac  failure. 

The  next  sign  to  appear  is  usually  an  increase  in  the  cardiac 
dullness  to  the  right  of  the  sternum — at  first  without  any 
discernable  pulsation ;  but  in  cases  showing  well-marked 
dilatation  some  pulsation  to  the  right  of  the  sternum  will 
be  noticeable. 

Before  the  dilatation  has  advanced  as  far  as  this  there 
will  probably  be  evidence  that  the  ventricle  is  dilating  down- 
wards as  well  as  to  the  right,  as  shown  by  the  appearance 
of  pulsation  in  the  epigastrium.  In  some  cases,  indeed,  the 
first  sign  may  be  the  appearance  of  palpable  or  visible  pulsation 
in  this  situation  under  the  lower  end  of  the  sternum.  When 
not  very  definite  this  may  be  best  detected  by  laying  the  hand 
flat  upon  the  lower  part  of  the  sternum  and  epigastrium — 
provided  of  course  that  the  palm  of  the  hand  has  been  educated 
for  purposes  of  palpation. 

When  dilatation  to  the  right  is  well  marked,  it  is  easily 
found  by  percussion,  if  looked  for ;  but  in  its  lesser  degrees 
it  may  be  necessary  to  percuss  the  chest  with  the  lungs  fully 
deflated  by  deep  expiration  before  it  is  possible  to  decide 
whether  the  right  side  of  the  heart  is  dilated  or  not.  If  a  certain 
amount  of  emphysema  be  present  it  will  most  likely  not  be 
possible  to  decide  with  certainty  whether  the  ventricle  is 
dflated  to  the  right  or  not.  Under  these  circumstances, 
however,  this  is  not  of  much  consequence  clinically,  because 
the  downward  displacement  of  the  heart  which  usually  accom- 
panies emphysema,  when  at  all  well  marked,  will  bring  the 
lower  part  of  the  ventricle  within  reach  of  palpation  in  the 
epigastrium,  and  the  amount  of  cardiac  failure  present  can 
be  estimated  by  the  amount  of  epigastric  pulsation  taken 
in  conjunction  with  the  amount  of  emphysema. 

When  speaking  of  the  dilatation  of  the  heart  to  the  right, 
which  is  noticeable  in  heart  failure,  nothing  so  far  has  been 


DILATATION  OF  AURICLE  41 

said  as  to  dilatation  of  the  right  auricle.  As  the  right  auricle 
lies  to  the  right  of  the  ventricle  it  would  naturally  be  supposed 
that  in  cases  of  tricuspid  regurgitation  part  of  the  increased 
area  of  dullness  to  the  right  of  the  sternum  would  be  due  to 
the  dilatation  of  the  right  auricle.  As  a  matter  of  clinical 
observation,  however,  it  is  extremely  rare  for  a  dilated  right 
auricle  to  come  sufficiently  near  to  the  anterior  chest  wall 
for  it  to  be  recognisable  by  palpation — or  even,  I  believe,  by 
percussion. 

During  the  last  twenty-five  years,  I  have  examined  with 
the  cardiograph  almost  every  case  I  have  met  with  where  it 
seemed  at  all  possible  that  pulsation  to  the  right  of  the  sternum 
was  due  to  the  right  auricle ;  but  with  only  two  or  three 
exceptions  the  cardiograph  has  shown  conclusively  that  the 
pulsation  was  due  to  the  right  ventricle  and  not  to  the 
auricle.  In  only  one  case  was  it  possible  to  obtain  true  auri- 
cular tracings,  and  in  another  case,  such  tracings  as  could  be 
got  suggested  that  the  faint  pulsation  observable  was  due  to  the 
dilatation  of  the  thin  membranous  part  of  the  auricle  near 
the  inferior  cava  rather  than  to  a  dilatation  of  the  muscular 
part  of  the  auricle  itself  {vide  pp.  339,  404,  and  Plate  XII). 

This  absence  of  auricular  pulsation  in  right -sided  dilatation 
of  the  heart  shows  that  dilatation  of  the  right  ventricle,  as  a 
rule,  precedes  dilatation  of  the  right  auricle.  The  stretching 
of  the  anterior  wall  of  the  right  ventricle  causes  the  auriculo- 
ventricular  groove  to  be  carried  so  far  to  the  right  of  its 
normal  position  that  the  whole  of  the  anterior  aspect  of  the 
dilated  heart  is  occupied  by  the  right  ventricle,  and  the  dilated 
auricle  projects  simply  towards  the  right  and  does  not  come 
into  relationship  to  the  anterior  chest  wall. 

Post-mortem  examination,  where  the  heart  is  flaccid  and 
undistended,  may  seem  to  controvert  this  statement ;  for  it 
may  seem  as  if  the  right  auricle  would  come  into  relationship 
to  the  anterior  chest  wall  during  life.  If,  however,  the  right 
ventricle  be  distended  by  injection  or  by  the  simple  and  easier 
method  of  inserting  a  deflated  thin  rubber  bag  (penny  toy 
balloon),  and  inflating  it  with  air  or  water  by  means  of  a  rubber 
tube,  it  can  easily  be  shown  that  the  above  statement  is  correct, 
in  the  very  great  majority  of  instances,  and  that  as  a  rule  the 


42  ADULT  TYPE  OF  DILATATION 

right  auricle  when  dilated  does  not  come  into  close  enough 
relationship  to  the  anterior  chest  wall  for  its  pulsation  to  be 
observable  clinically,  but  that  the  pulsating  portion  of  the 
right  heart  is  almost  invariably  the  right  ventricle. 

Although  a  dilated  right  auricle  does  not,  as  a  rule,  give 
signs  recognisable  by  palpation  on  percussion  anteriorly  it 
may  reveal  its  presence  to  auscultation  posteriorly ;  for  an 
abnormal  distinctness  in  the  cardiac  sounds  or  murmurs,  as 
heard  over  the  lower  right  interspaces  near  the  spine  pos- 
teriorly, is  often  noticeable  in  cases  where  the  right  auricle 
is  in  all  probability  dilated.  Such  an  increased  loudness  is 
to  be  expected  owing  to  the  anatomical  position  of  the  right 
amicle. 

Auscultation  in  heart  failure  where  the  heart  is  of  moderate 
distensibility. — The  information  given  by  auscultation  in 
cases  of  right  ventricular  failure  is  very  valuable,  and  in  middle 
and  later  life  it  has  to  be  relied  upon  more  than  percussion 
or  palpation.  In  adolescence,  we  saw  that  this  w^as  not  so, 
and  that  palpation  and  percussion  were  of  more  diagnostic 
value  than  auscultation. 

In  the  early  stages  of  failm-e,  important  information  can 
be  gathered  from  the  relative  loudness  of  the  heart  sounds 
as  heard  at  the  apex  (over  the  left  ventricle)  and  over  the 
right  ventricle  between  the  sternum  and  the  nipple  line.  The 
loudness  of  the  pulmonary  second  sound  is  also  a  very  valu- 
able guide  to  the  amount  of  work  wliich  the  right  heart  is 
doing,  and  its  loudness  over  its  point  of  maximal  intensity 
in  the  second  or  third  interspaces  and  over  the  body  of  the 
right  ventricle  must  be  compared  with  the  normal  and  with 
the  loudness  of  the  second  sound  as  heard  at  the  apex,  w'hich 
is,  as  a  rule,  entirely  due  to  the  aortic  portion  of  the  second 
sound.  The  loudness  of  the  second  sound,  as  heard  in  the 
aortic  area,  while  of  considerable  cHnical  value,  is  not  of  so 
much  service  for  the  comparative  observations  here  spoken 
of,  because  its  loudness  is  more  dependent  upon  the  condition 
and  amount  of  the  overlying  lung — factors  whose  exact  value 
it  is  not  always  easy  to  estimate. 


AUSCULTATION  43 

Murmurs  due  to  Tricuspid  Eegurgitation 

Of  the  murmurs  which  are  due  to  tricuspid  regurgitation, 
the  most  generally  recognised  is  the  systolic  murmur  produced 
at  the  tricuspid  orifice ;  but  it  must  be  remembered  that, 
while  this  is  a  very  valuable  evidence  of  regurgitation,  when 
present,  its  absence  is  of  no  value  as  negative  evidence  ;  for  it 
is  extremely  common  for  well-marked  tricuspid  regurgitation 
to  be  unaccompanied  by  this  systolic  murmur. 

The  Tricuspid  Systolic  Murmur. — As  regards  its  char- 
acteristics :  its  tone  is  somewhat  lower  as  a  rule  than  that 
of  the  mitral  systolic  murmur,  as  might  be  expected  from 
the  lower  blood  pressure  on  the  right  side  of  the  heart  as 
compared  with  the  left. 

Its  point  of  maximal  loudness,  when  not  very  well  marked, 
is  usually  over  the  fourth  and  fifth  interspaces  just  to  the 
left  of  the  sternum.  Since  the  regurgitant  stream,  producing 
the  murmur,  is  flowing  towards  the  right  into  the  auricle, 
it  might  be  expected  that  the  murmur  would  be  first  and  best 
hoard  to  the  right  of  the  sternum.  This  is,  however,  not  so 
clinically,  and  the  reason  is  that  already  given  when  speaking 
of  the  auricle  in  relation  to  palpation  and  percussion — namely, 
that  it  does  not,  as  a  rule,  come  near  the  anterior  chest  wall. 

The  ordinary  rule  as  to  the  conduction  of  murmurs  does, 
however,  hold  good  for  tricuspid  regurgitation,  as  is  shown 
by  the  rare  cases  where  the  right  auricle  can  be  examined. 
In  the  only  case  I  have  seen,  not  only  was  the  tricuspid  murmur 
very  loudly  conducted  into  the  auricle,  but  the  impact  of  the 
regurgitating  blood  was  so  forcible  upon  its  antero-lateral 
wall  that  a  very  well-marked  systolic  thrill  could  be  felt  in 
the  fourth  right  interspace  internal  to  the  nipple  line.  This 
thrill  had  its  point  of  maximal  intensity  just  internal  to  the 
nipple  where  the  regurgitant  stream  of  blood  might  be  expected 
to  strike  the  wall  of  the  auricle. 

When  the  murmur  is  louder  its  area  of  audition  is  an 
elongated  oval  reaching  from  about  the  tliird  rib  above  to 
the  sixth  rib  or  so  below,  and  from  the  left  lateral  edge  of  the 
sternum  nearly  to  the  left  nipple  hne.  When  louder  still,  the 
area  broadens  to  the  right,  embracing  the  whole  of  the  sternum 


44  ADULT  TYPE  OF  DILATATION 

and  also  becoming  audible  to  the  right  of  it  {vide  figs.  76  and 
110).  When  heard  as  widely  as  this,  the  true  systolic  tricuspid 
becomes  merged  with  the  next  murmur  of  which  we  have  to 
speak,  although  the  two  may  still  be  more  or  less  distinguishable 
by  a  difference  in  tone. 

The  tricuspid  murmur  is,  when  well  marked,  often  audible 
downwards  and  to  the  right  over  the  line  of  the  inferior  cava 
and  the  hepatic  vein,  and  this  direction  of  conduction  is  some- 
times of  value  for  its  identification  when  other  murmurs  are 
present.  The  fact  that  on  listening  downwards  and  to  the 
right  the  murmur  retains  its  distinctness  as  compared  with 
the  first  sound  of  the  heart  may  be  taken  as  strong  evidence 
that  a  tricuspid  systolic  murmur  is  present.  If,  on  the  other 
hand,  on  listening  in  this  direction  the  distinctness  of  the  murmur 
is  lost  more  rapidly  than  the  distinctness  of  the  first  sound 
of  the  heart,  it  is  highly  probable  that  the  murmur  has  its 
point  of  origin  farther  away  than  the  right  ventricle,  and  is  a 
loudly  conducted  mitral  or  other  systolic  murmur  {vide  p.  279). 

When  the  tricuspid  regurgitation  is  considerable  enough  to 
cause  a  well-marked  systolic  impulse  in  the  veins,  the  murmur 
will  be  well  conducted  into  the  veins  of  the  neck  and  will 
merge  into  the  murmur  to  be  next  described. 

The  Superior  Vena  Cava  Murmur  of  tricuspid  re- 
gurgitation.— In  addition  to  the  ordinarily  described  murmur 
of  tricuspid  regurgitation,  there  is  another  one  which  is  not 
as  yet  generally  recognised,  although  it  is  of  very  common 
occurrence  and  is  of  very  considerable  diagnostic  value. 

The  murmur  in  question  is  produced  in  the  superior  vena 
cava  at  the  point  where  it  passes  through  the  pericardium, 
and  it  can  only  occur  when  there  is  sufficient  regurgitation 
to  cause  marked  distension  of  the  vein  above  and  below 
this  point. 

When  the  vein  is  distended,  the  strengthening  of  its  walls 
by  the  fibrous  tissue  of  the  pericardium,  at  the  spot  where 
it  passes  through  that  structure,  will  Hmit  the  amount  of 
dilatation  in  this  situation,  thus  causing  somewhat  of  a  con- 
striction in  the  dilated  vein.  The  distension  of  a  dilated 
superior  vena  cava,  with  hard  paraffin,  prior  to  the  removal 
of  the  heart  from  the  body,  readily  demonstrates  this  narrowing 


VENA  CAVA  MURMUR  45 

of  the  dilated  vein,  and  shows  it  to  be  sufficient  in  extent  to 
cause  a  murmur  as  the  regurgitating  blood  rushes  through 
into  the  more  dilated  vessel  beyond. 

Before  noticing  this  peculiarity  of  a  dilated  superior  cava, 
some  twenty  years  ago,  I  had  already  come  to  recognise  the 
presence  of  a  systolic  murmur  audible  in  cases  of  tricuspid 
regurgitation  whose  point  of  maximal  loudness  was  much  to 
the  right  of  that  of  the  true  tricuspid  systolic  murmur,  and 
the  discovery  of  the  above-named  peculiarity  of  a  dilated 
superior  vena  cava  showed  how  such  a  murmur  might  be 
produced. 

Increased  famiharity  with  this  systoHc  murmur  of  venous 
origin  has  only  confirmed  my  early  observations  and  convinced 
me  that  there  is  justification  for  calling  it  the  superior  vena 
cava  murmur. 

As  regards  tone,  it  closely  resembles  that  of  the  true  tri- 
cuspid systolic,  and  when  both  murmurs  are  present,  the  only 
means  of  deciding  as  to  its  presence  or  absence  is  by  noting 
whether  there  is  or  is  not  a  second  point  of  maximal  intensity 
over  the  situation  of  the  portion  of  the  superior  cava  where 
the  murmur  is  produced. 

It  is  by  this  point  of  maximal  loudness  or  intensity  (its 
'  P.M.I.')  that  this  murmur  is  best  recognised,  and  by  this 
it  is  distinguished  from  the  tricuspid  systolic  murmur.  It  is 
heard  best  to  the  right  of  the  sternum  over  the  higher  inter- 
spaces— usually  the  third  and  fourth,  or  the  second  and  third — 
and  usually  it  rapidly  lessens  in  loudness  on  listening  more 
than  an  inch  from  the  sternum. 

Sometimes  the  maximal  loudness  is  higher — namely,  in  the 
second  and  first  interspaces — and  when  this  is  the  case  the 
murmur  will  very  easily  be  mistaken  for  one  of  aortic  origin, 
owing  not  only  to  its  P.M. I.,  but  also  to  the  fact  of  its  conduc- 
tion along  the  vessels.  When  a  thrill  is  present  in  the  veins,  as 
occurs  in  some  cases  of  extreme  tricuspid  regurgitation — the 
similarity  between  the  two  murmurs  is  very  close — moreover, 
the  strongly  pulsating  veins  may  simulate  the  pulsating 
arteries  of  aortic  regurgitation  {vide  Essay  IV,  p.  220  and  222). 

This  murmur,  when  accompanied  by  a  true  systolic  tricuspid 
murmur,  is  easy  of  recognition,  for  it  is  not  at  all  well  conducted 


46  HEART  FAILURE  IN  ADULT  LIFE 

downwards,  and  is  often  not  heard  at  all  over  the  cardiac  area 
below  the  level  of  the  fourth  rib,  neither  is  it  conducted  towards 
the  liver.  (For  the  further  discussion  of  this  murmur,  vide 
p.  218.)  The  recognition  of  this  murmur  often  gives  very 
useful  clinical  information.  For  example,  in  the  absence  of  re- 
cognisable dilatation  of  the  heart  and  of  a  true  tricuspid  systolic 
murmur,  its  occurrence  shows  that  there  is  really  considerable 
dilatation  of  the  superior  cava.  Moreover,  its  absence  gives 
more  certain  evidence  as  to  the  absence  of  tricuspid  regurgitation 
than  does  the  absence  of  the  true  tricuspid  systolic  murmur. 

The  other  auscultatory  phenomena  observable  in  cases  of 
this  type  of  dilatation  of  the  right  ventricle  are  of  less  clinical 
value,  and  as  they  will  be  fully  discussed  subsequently,  they 
need  only  be  mentioned  here.  They  are  a  third  sound  produced 
in  the  right  ventricle,  and  sometimes  a  right  ventricular 
mid-diastolic  murmur.  These  are  most  frequently  noticed 
in  cases  with  anaemia,  and  will  be  dealt  with  when  heart 
failure  in  anaemia  is  discussed  {vide  p.  282). 

When  the  diagnostic  difficulties  associated  with  dilatation 
of  the  right  ventricle  are  taken  up,  the  occurrence  of  a  thrill 
in  the  veins  due  to  tricuspid  regurgitation  and  also  the 
occurrence  of  a  sound  due  to  closure  of  the  venous  valves 
or  to  murmurs  produced  by  their  incompetence  will  be  referred 
to  {vide  pp.  219  and  220). 

Changes  in  the  Left  Ventricle  in  Heart  Failure  with 
Enlargement 

When  speaking  of  the  distensible  heart  of  adolescence 
changes  in  the  left  ventricle  were  not  touched  upon  because 
the  relative  weakness  of  the  right  heart  in  these  cases  pre- 
vented any  early  changes  from  taking  place  in  the  left.  In 
anaemia  this  is  especially  the  case,  and  even  in  simple  over- 
strain a  very  considerable  degree  of  heart  failure  with  breath- 
lessness  can  exist  without  any  signs  pointing  definitely  to 
left-side  failure. 

In  the  less  distensible  heart  of  middle  life,  however,  this 
same  disparity  does  not  exist,  and  we  expect  to  find  some 
evidence  of   left-ventricle  failure  in  everv  well-marked    case 


LEFT  VENTRICULAR  CHANGES         47 

of  cardiac  failure  through  overstrain,  and  sometimes  the  two 
sides  of  the  heart  appear  to  be  equally  affected  quite  early  on. 

In  this  connection  it  must  not  be  forgotten  that  the  most 
distensible  basal  portion  of  the  left  ventricle  lies  deeply  in  the 
thorax,  and  therefore  changes  due  to  dilatation  may  not  show 
until  they  are  well  marked. 

Firstly,  as  regards  the  pulmonary  veins.  The  only  means 
we  have  of  judging  as  to  their  condition  is  by  noting  the  amount 
of  work  which  the  right  ventricle  is  doing ;  and  where  we  find 
distinct  evidence  that  the  right  heart  is  doing  an  abnormal 
amount  of  work,  as  judged  by  the  loudness  of  its  soimds  and 
an  increase  in  the  amount  of  its  pulsation,  we  are  justified 
in  inferring  early  failure  of  the  left  ventricle — provided  that 
it  is  possible  to  exclude  wdth  reasonable  certainty  any 
hindrance  to  the  circulation  of  pulmonary  origin,  such  as 
emphysema,  anaemia,  &c. 

As  regards  the  left  amicle,  it,  too,  is  of  little  value  to  us 
clinically  as  a  guide  to  the  condition  of  the  ventricle  from  the 
point  of  view  of  the  early  diagnosis  of  heart  failure,  because 
of  its  being  on  the  posterior  aspect  of  the  heart ;  nevertheless, 
it  may,  when  much  dilated,  give  some  evidence  both  to  per- 
cussion and  auscultation,  for  under  these  chcumstances  it  may 
show  some  recognisable  dullness  in  the  left  interscapular  region 
— as  described  by  Dr.  Ewart ;  and  on  listening  in  this  region 
it  is  often  possible  to  notice  that  the  heart  sounds  are  clearly 
audible,  whereas  normally  they  are  usually  not  heard. 

The  abnormal  conduction  of  the  heart  sounds  to  the  back 
in  this  situation  may  be  taken  as  pointing  to  dilatation  of 
the  am-icle,  and  this  is  often  of  value  as  a  confii-matory  sign 
of  dilatation,  for  it  is  noticeable  with  an  amount  of  dilatation 
insufficient  to  cause  any  percussion  dullness. 

As  to  the  left  ventricle  itself,  the  two  chief  signs  of  failure 
with  enlargement  are  displacement  outwards  and  downwards 
of  the  apex  and  the  presence  of  a  mitral  systohc  murmur. 
As  regards  the  displacement  of  the  apex,  it  is  sometimes 
said  that  hypertrophy  wdth  dilatation  causes  an  enlargement 
of  the  heart  which  carries  the  apex  downwards  and  outwards 
in  equal  proportions,  and  therefore  by  causing  a  uniform 
aymmetrical  enlargement  maintains  the  apex  in  the  same  axis 


48  HEAKT  FAILURE  IN  ADULT  LIFE 

as  before  ;  in  dilatation  without  hypertrophy,  on  the  other 
hand,  there  is  more  broadening  of  the  ventricle,  and  therefore 
the  apex  is  carried  rather  more  outwards  than  downwards, 
and  so  takes  up  a  position  to  the  left  of  the  normal  axis. 
Although  this  may  be  so,  to  some  extent,  the  broadening  is 
more  apt  to  be  marked  above  the  apex  than  to  involve  the 
apex  itself.  As  regards  the  signs  of  heart  failure  given  by  the 
loudness  of  the  left  ventricular  sounds,  no  generalisation  can 
be  made,  because  if  the  failure  be  due  to  muscular  weakening 
from  nervous  or  nutritional  causes,  the  sounds  will  become 
weaker  and  shorter  and  wanting  their  full  tone.  If  on  the 
other  hand  it  is  because  of  absolute  overstrain  from  rise  in 
arterial  resistance  or  excessive  exertion,  the  heart  failure  may 
be  accompanied  by  undue  loudness.  But  if,  as  is  possible,  these 
two  factors  be  nicely  balanced,  heart  failure  may  be  accom- 
panied by  absolutely  normal  loudness  of  the  heart  sounds. 

It  is  not  until  the  ventricle  is  sufficiently  dilated  to  produce 
some  incompetence  of  the  mitral  valve  that  we  have  the  first 
unequivocal  sign  of  left  ventricular  dilatation — namely,  the 
mitral  systolic  murmur. 

It  is  sometimes  not  easy  to  decide  whether  a  faint  murmur 
at  the  apex  be  really  due  to  mitral  regurgitation  or  not ;  but 
this  point  can  usually  be  definitely  cleared  up  by  noting  the 
way  in  which  the  murmur  is  conducted  towards  the  axilla 
as  compared  with  the  conduction  of  the  first  sound.  If  the 
murmur  arise  at  the  mitral  valve  it  will  retain  its  relative 
loudness  as  compared  with  the  first  sound. 

If  the  murmur  be  fainter  than  the  first  sound,  as  heard 
at  the  apex,  when  listening  farther  and  farther  out,  a  point 
may  be  reached — say,  in  the  mid-  or  the  posterior-axillary 
line — when  the  first  sound  only  is  audible  and  not  the  murmur ; 
but,  nevertheless,  the  gradual  and  equal  diminution  in  the 
loudness  of  the  two  sounds,  until  the  one  is  too  faint  to  be 
heard,  shows  that  they  both  arise  at  the  same  valve  and 
that  the  murmur  is  really  a  mitral  systolic. 

Again,  supposing  they  are  equally  loud :  the  fact  that  the 
murmur  is  audible  wherever  the  left  ventricle  first  sound  is 
audible  wall  prove  its  mitral  origin. 

But,  on  the  other  hand,  supposing  that  the  murmur  is 


LEFT  VENTRICULAE  CHANGES  49 

fairly  loud  at  the  apex,  but  that  on  listening  towards  the 
axilla  it  rapidly  becomes  famter  and  is  lost,  while  the  first 
sound  remains  fairly  loud,  the  diagnosis  can  certainly  be 
made  that  this  is  not  a  mitral  murmm-  showing  incompetence 
of  the  valve. 

The  diagnosis  of  one  of  the  most  puzzling  forms  of 
cardio-respiratory  murmur  depends  upon  this  method.  Some- 
times a  murmur  exactly  resembling  a  mitral  systolic  murmur 
is  caused  by  pressure  of  the  apex  of  the  heart  upon  the 
adjacent  lung,  and  it  may  even  continue  to  be  produced  when 
the  breath  is  held.  Careful  study,  however,  of  its  loudness 
in  relation  to  that  of  the  first  somid  \vill  show  that  its  point 
of  maximal  loudness  is  some  inch  or  so  external  to  that  of 
the  first  sound.  On  studying  the  conduction  of  this  murmur, 
outwards  from  the  apex  (where  the  first  sound  is  loudest) 
towards  the  axilla,  it  will  be  found  that  it  increases  in  loudness 
for  the  first  mch  or  so — i.e.,  until  a  certain  amount  of  lung 
intervenes  between  the  stethoscope  and  the  heart — showing 
that  the  murmur  arises  in  this  portion  of  the  lung  and 
not  in  the  heart  itself.  In  such  a  case,  although  the 
murmur  may  be  audible  round  to  the  back  and  the  angle  of 
the  scapular,  its  pulmonary  origin  can  be  proved  by  watching 
the  way  the  point  of  maximal  intensity  shifts  during  full 
inspiration  and  full  expiration — always  keeping  an  inch  or  so 
away  from  the  uncovered  portion  of  the  heart  and  never  heard 
best  over  the  heart  itself  {vide  p.  446). 

As  regards  the  sequence  of  the  phenomena  showing  heart 
failure  in  moderately  distensible  hearts,  it  is  not  possible  to 
make  any  useful  generalisation  as  was  the  case  in  adolescence, 
because  the  mode  of  onset  is  so  liable  to  vary,  according  to 
the  degree  of  distensibihty  which  the  heart  possesses.  The 
chief  guides  are  the  well-knowTi  ones — ^namely,  the  amount  and 
nature  of  the  venous  pulsation  in  the  neck,  the  amount  of 
dilatation  of  the  heart  to  the  right  and  to  the  left,  and  the 
presence  or  absence  of  a  mm-mm-  due  to  tricuspid  regm-gitation, 
produced  either  at  the  valve  itself  or  in  the  superior  cava,  and 
the  presence  or  absence  of  a  mitral  systoKc  mmmur.  The 
presence  of  epigastric  pulsation,  and  enlargement  and  pulsation 
of  the  liver,  must  also  be  looked  for  and  its  degree  noted. 


50  HEAKT  FAILURE 


Heart  Failure  without  Enlargement 

We  now  come  to  the  second  main  group  into  which  it  is 
necessary  to  divide  all  cases  of  heart  failure.  In  the  group 
with  enlargement  just  discussed  it  was  pointed  out  that  dila- 
tation could  only  occur  provided  that  the  internal  pressure 
which  the  heart  muscle  could  develop  was  in  excess  of 
the  resisting  power  of  the  weakest  portion  of  the  ventricle 
walls. 

As  soon  as  these  conditions  are  not  fulfilled,  owing  to 
abnormal  weakness  of  the  heart  muscle  or  abnormal  resisting 
power  on  the  part  of  the  heart  walls,  failure  with  enlargement 
is  no  longer  possible,  and  heart  failure  without  enlargement 
will  occur  instead. 

It  may  perhaps  be  objected  that  where  the  heart  muscle 
reaches  this  degree  of  relative  weakness  the  circulation  cannot 
be  carried  on  and  death  must  occur ;  but  this  objection  is 
answered  by  clinical  observations  which  show  that  there  is 
a  fairly  wide  margin  between  these  two  alternatives,  and  that 
life — and  sometimes  a  fairly  active  life — is  possible  under  these 
circumstances. 

This  group  must  be  divided  up  into  two  sub-groups  according 
to  the  distensibihty  possessed  by  the  heart ;  for  here,  even  more 
than  in  the  last  group,  the  signs  and  symptoms  of  cardiac 
failure  depend  upon  the  degree  of  elasticity  of  the  heart,  and 
the  phenomena  observable  in  the  muscularly  weak  adolescent 
heart  are  quite  different  from  those  seen  in  the  relatively 
rigid  heart  of  old  age. 

In  this  case  there  will  be  no  need,  as  in  the  last  instance, 
to  discuss  the  subject  under  three  headings,  according  to  the 
degree  of  distensibihty  which  the  heart  possesses,  because 
hearts  of  moderate  distensibihty  do  not  show  phenomena 
differing  from  those  at  the  two  extreme  ends  of  the  series, 
but  only  a  combination,  to  a  varying  extent,  of  these 
phenomena. 

In  approaching  this  subject  one  of  two  courses  might  be 
taken  :  either  the  reader  might  be  led  step  by  step  through 
the  clinical  observations  which  led  the  writer  up  to  the  theo- 


WITHOUT  ENLARGEMENT  51 

retical  considerations  which  will  here  be  given  (and  it  is  of 
interest  to  note  that  some  of  the  most  obvious  of  these  latter 
were  the  last  instead  of  the  first  to  be  deduced  from  the  clinical 
facts)  ;  the  other  course,  and  probably  the  best  one,  is  to 
present  the  subject  as  complete  as  possible  from  a  cHnical  and 
theoretical  point  of  view,  irrespective  of  the  stages  the  writer 
passed  through  in  the  evolution  of  the  theory  here  given. 

To  take  the  second  of  these  two  courses  will  probably 
give  the  most  generally  useful  review  of  the  changes  in  the 
heart  with  which  it  is  now  proposed  to  deal. 

Take  now  the  case  of  an  elastic,  distensible  heart — such  as 
is  found  in  an  adolescent  of  the  age,  say,  of  sixteen  or  seventeen. 
We  have  discussed  wdiat  happened  when  the  intraventricular 
pressure,  owing  to  muscular  weakness,  falls  so  much  below 
its  normal  level  that  it  is  no  longer  able  to  expel  the  normal 
contents  against  the  pressure  which  it  has  to  face  in  the 
arteries. 

Let  us  take  the  case  of  the  left  ventricle  in,  say,  a  case  of 
rheumatic  myocardial  weakness  or  in  the  toxic  heart  failure 
that  occurs  after  influenza  or  diphtheria. 

As  soon  as  the  muscular  power  falls  so  low  that  it  caimot 
expel  the  normal  ventricular  charge  (of  about,  say,  3  ounces  of 
blood)  against  the  resistance  it  has  to  face  in  the  aorta,  one 
of  two  things  must  happen :  either  the  patient  must  die  of 
asystole  or  nature  must  find  some  means  of  lessening  the 
load  proportionally  to  the  muscular  power  of  the  heart. 

Now,  if  the  physical  and  physiological  conditions  we  are 
dealing  with  be  looked  into,  a  way  out  of  the  difficulty  is 
evident ;  for  it  is  clear  that  a  muscular  chamber  which  cannot 
commence  the  act  of  emptying  itself  when  it  is  full  and  its 
muscular  fibres  are  fully  stretched,  might  nevertheless  be  able  to 
do  so  when  it  was  not  so  fully  distended  and  the  muscular  fibres 
of  its  walls  were  able  to  support  one  another  more.  The 
muscular  walls  of  a  partially  filled  ventricle  are  thicker,  and 
therefore  presumably  more  effective,  than  those  of  a  fully 
distended  one. 

It  is  probable  also  that  the  principle  of  the  hydraulic 
press  applies  here  to  some  extent,  and  that,  taking  the  diameter 
of  the  aorta  as  a  fixed  quantity,  the  ease  with  which  the 

e2 


52  HEART  FAILURE 

vontriclu  empties  itself  into  the  aorta  will  be  proi^ortional  to 
the  smallness  of  its  sectional  area  as  compared  with  that  of 
the  aorta. 

Apart  from  these  theroretical  considerations  the  clinical 
fact  is  certain  that  in  cases  of  extreme  myocardial  failm*e 
the  heart  does  diminish  in  size,  and  the  volume  of  the  thoracic 
contents  and  of  the  liver  also  diminish,  thus  showing  a  diminu- 
tion in  the  amount  of  blood  which  the  heart  is  able  to  keep  in 
active  ckculation. 

The  mechanism  whereby  this  diminution  is  brought  about 
is  quite  simple,  for  those  who  hold — as  the  writer  has  done 
for  more  than  a  quarter  of  a  century — that  the  ventricle 
fills  itself  by  an  act  of  true  muscular  expansion,  or,  in  other 
words,  that  the  ordinary  longitudinal  contraction  of  the  mus- 
cular fibres  is  followed,  in  the  shortened  and  broadened  fibres, 
by  a  transverse  contraction  whose  effect  is  suddenly  to  restore 
the  fibre  to  the  condition  it  was  in  prior  to  the  contraction. 

In  the  adolescent,  as  has  already  been  pointed  out,  the 
fibrous  elements  of  the  heart  are  soft  and  possess  a  maximal 
degree  of  distensibility  and  a  minimal  degree  of  rigidity ; 
therefore  in  adolescence  their  power  of  resisting  deformation 
must  be  at  its  minimum,  and  the  heart  will  have  but  little 
tendency  to  return  to  its  former  shape,  after  contraction,  in 
virtue  of  its  elastic  recoil  alone. 

Therefore,  the  heart's  power  of  meclianical  aspiration,  after 
contraction,  will  not  be  great,  and  the  heart  will  have  to 
depend  mainly  upon  its  muscular  power  for  the  expansile 
force  whereby  it  fills  itself. 

Now  in  the  cases  we  are  considering,  the  muscles  have 
lost  much  of  their  contractile  power  through  inflammatory 
or  other  damage,  and  this  being  so  their  muscular  expansile 
power  must  also  have  suffered.  In  these  facts,  I  think  we 
can  see  the  means  whereby,  in  severe  myocardial  failure,  the 
work  of  the  heart  is  compensatorily  cut  down  proportionally 
to  the  muscular  weakening.  The  same  heart  weakness  which 
prevents  the  heart  fi'om  emptying  itself,  also  prevents  it  from 
filling  itself. 

This  statement  ought,  however,  to  be  reversed,  and  read 
thus  :— 


WITHOUT  ENLARGEMENT  53 

The  first  result  of  extreme  muscular  weakness  in  a  heart 
whose  fibrous  tissues  are  soft  and  possess  little  resisting  power 
is  that  the  heart  is  unable  properly  to  fill  itself,  because  its 
power  of  filling  itself  is  dependent  solely  upon  the  aspiratory 
force  which  the  active  expansion  of  its  muscular  walls  can 
develop.  By  this  failure  to  fill  itself  properly  the  heart  is 
largely  safeguarded  against  the  risk  of  asystole,  for  the  amount 
of  blood  which  the  heart  draws  into  itself  is  proportional  to 
the  amount  which  it  is  capable  of  expelling. 

As  the  expansion  movement  is  a  weaker  one  than  con- 
traction, suction  will  fail  sooner  than  expulsion,  and  there- 
fore there  is  no  Hkelihood  of  the  heart  drawing  into  itself  more 
blood  than  it  is  able  to  expel. 

To  those  who  do  not  fully  accept  the  muscular-expansion, 
theory  this  diminution  in  the  volume  of  the  heart  and  of  the 
blood  in  active  circulation  is  also  explicable ;  for  the  gi-adual 
onset  of  muscular  weakness  will  limit  the  volume  of  the  cir- 
culation. The  weakness  of  the  right  ventricle  will  lessen  the 
volume  of  the  pulmonary  circulation  and,  as  a  consequence, 
the  amount  of  blood  available  for  the  filling  of  the  left  heart 
will  also  be  lessened,  and  the  deficient  amount  of  blood  forced 
into  the  systemic  circulation  will  presumably  lessen  the  venous 
return  to  the  right  ventricle,  an  abnormal  amount  of  blood 
being  left  in  the  venous  reservoirs. 

In  the  distensible  heart  of  adolescence  this  is  what  takes 
place  when  severe  myocardial  failm-e  sets  in,  and  this  is  the 
reason  for  the  smallness  of  the  heart  and  the  diminution  in 
the  size  of  the  vascular  organs,  lungs,  and  liver,  which  is 
clinically  observable  in  such  cases  {vide  pp.  68,  118,  180,  185). 

In  contrast  with  these  cases,  let  us  briefly  review  what  takes 
place  in  a  heart  whose  tissues  have  attained  to  the  increased 
rigidity  which  comes  with  advancing  years.  In  such  a  heart, 
w^e  are,  I  think,  justified  in  expecting  that  the  non-muscular 
portion  of  the  heart  has  more  power  of  resisting  deformation 
than  is  the  case  in  the  still  gi-owuig  heart  of  adolescence  : 
in  other  words,  in  the  adult  the  heart  not  only  possesses 
the  power  of  enlarging  itself  by  its  muscular  recoil  movement, 
but  also  tends  to  return  to  it  original  size  after  contraction 
by  reason  of  a  mechanical  elastic  recoil  as  well. 


54  HEART  FAILURE 

Therefore,  in  the  adult,  weakening  of  the  heart  muscle  inter- 
feres with  its  expulsive  power  more  than  it  does  with  its 
aspiratory  power,  and  a  weak  heart  is  able,  by  virtue  of  its 
mechanical  elastic  recoil,  to  draw  into  itself  a  larger  charge 
than  its  muscular  power  is  able  to  expel.  This  is,  in  my 
opinion,  the  explanation  of  the  well-known  fact  that  sudden 
death  from  asystole  is  a  far  more  common  result  of  muscular 
weakness  in  later  life  than  it  is  in  early  life. 

Before  going  further  into  this  latter  question,  however, 
the  simpler  subject  of  heart  failure  in  distensible  hearts  will 
be  discussed. 

Heart  Failure  with  Small  Heart 

In  the  type  of  heart  we  are  now  dealing  with,  well-marked 
muscular  failure  of  the  heart  is  usually  associated  with  an 
actual  diminution  in  its  size,  so  far  as  it  is  clinically  observable, 
and  therefore  the  term  '  heart  failure  with  small  heart  '  is 
applicable  to  cases  in  this  group.  This  fact  was  first  brought 
to  the  writer's  notice  by  the  careful  study  of  the  size  of  the 
heart  and  liver  in  cases  of  malnutrition,  as  is  recounted  in 
Essay  II,  and  by  finding  that  the  starvation  necessary  for  the 
treatment  of  gastric  ulcer  did  cause  a  shrinkage  of  the  more 
elastic  of  the  vascular  organs,  betokening  a  diminution  in 
the  amount  of  blood  filhng  them,  and  therefore  in  the  total 
volume  of  the  blood.  From  this,  he  was  led  on  to  the  observa- 
tion that  a  similar  diminution  in  the  size  of  the  liver  and  the 
lungs  and  also  of  the  heart  was  noticeable  in  cases  where  the 
heart  was  muscularly  too  feeble  to  keep  a  normal  amount  of 
blood  in  circulation.  The  theoretical  considerations  here  given 
were  only  slowly  arrived  at  after  the  certainty  of  the  diminu- 
tion in  the  size  of  the  heart  and  in  the  volume  of  the 
circulation  was  evident  as  a  clinical  fact. 

When,  therefore,  we  are  speaking  of  distensible  hearts,  it 
can  be  asserted  that  *  whenever,  owing  to  muscular  weak- 
ness, the  expulsive  power  falls  below  the  resisting  power  of 
the  weakest  portion  of  the  ventricle  walls  heart  failure 
occurs  without  dilatation ;  and,  further,  whenever  the  expul- 
sive power  of  the  ventricle  falls  below  the  resistance  to  be 


WITH  SMALL  HEART  55 

overcome  in  the  aorta,  diminution  in  the  amount  of  the 
filhng  of  the  heart  will  take  place,  together  with  a  lessening  of 
the  total  amount  of  blood  in  active  circulation — a  condition 
well  described  as  '  heart  failure  with  small  heart.' 

This  gi'oup  of  cases  of  heart  failiu'e  with  small  heart  is  not 
a  large  one,  but  embraces  a  by  no  means  unimportant  type 
of  case,  where  there  is  extreme  muscular  weakness,  due  to 
such  causes  as  myocarditis,  toxaemic  poisoning  from  such 
diseases  as  rheumatism,  diphtheria,  influenza,  &c.  To  some 
clinicians  the  occurrence  of  such  a  group  at  all  may  be  a  matter 
of  doubt ;  but  if  they  will  only  follow  the  arguments  and  the 
clinical  observations  detailed  in  this  and  the  succeeding  essays 
and  examine  carefully,  for  themselves,  cases  similar  to  those 
recorded  here,  the  existence  of  this  group  will  become  for 
them  a  matter  of  the  same  certainty  as  it  is  in  the  case  of  the 
writer. 

The  careful  study  of  the  state  of  the  circulation  and  of 
the  size  of  the  heart,  and  of  the  more  elastic  and  vascular 
of  the  viscera,  in  cases  of  extreme  heart  weakness,  shows  quite 
conclusively  the  presence  of  phenomena  which  indicate  clearly 
that  the  total  volume  of  the  blood  circulated  by  the  heart 
has  been  compensatorily  lessened,  thus  making  it  better 
proportioned  to  the  lessened  cardiac  strength. 

When  the  heart  becomes  too  weak,  owing  to  extreme 
muscular  failure,  to  keep  the  normal  amount  of  blood  in 
active  circulation  a  certain  amount  is  cut  out  by  the  compensa- 
tory mechanism  akeady  described,  and  only  an  amount  such 
as  the  heart  can  cope  with  is  retained  in  the  mam  arteries 
and  veins. 

^^^lat  happens  to  the  remainder  of  the  blood  cannot  be 
definitely  stated,  but  no  doubt  it  is  stored  up  in  the  usual 
reservoirs  where  reserve  blood  is  kept  (namely,  the  abdominal 
and  other  plexuses  of  veins)  until  such  time  as  the  heart  recovers 
itself.  Or,  in  the  case  of  persisting  muscular  weakness,  until 
a  compensatory  diminution  in  the  total  blood  volume  can  be 
estabUshed.  The  theoretical  consideration  of  this  subject  is 
dealt  with  in  succeeding  essays  and  also  the  clinical  evidence 
that  there  is  a  diminution  in  the  size  of  organs — such  as  the 
lungs  and  liver — in  cases  of  extreme  muscular  w^eakness  of  the 


56  HEART  FAILURE 

heart ;  therefore,  the  chnical  features  only  of  extreme  heart 
failure  with  small  heart  will  be  here  discussed. 

Before,  however,  taking  up  the  early  signs  of  this  type  of 
heart  failure  it  will  be  well  to  discuss  its  clinical  characteristics, 
where  fully  estabhshed,  in  order  that  a  fairly  complete  clinical 
picture  of  the  heart  and  circulation  may  be  given. 

A  careful  examination  of  the  heart  and  circulation  in  a 
well-marked  case  of  extreme  muscular  asthenia,  from  such 
a  cause  as  myocarditis  or  toxaemia  accompanying  rheumatic 
fever,  or  following  such  a  condition  as  influenza  or  diphtheria, 
will  bring  out  some  or  all  of  the  following  phenomena.  Firstly, 
as  regards  general  and  well-known  signs.  The  pulse  will 
become  weak  and  small.  The  heart  sounds  will  lessen  in 
loudness  and  vigour,  and  the  apex  beat  will  become  faint  or 
indistinguishable. 

Amongst  the  more  important  of  the  less-known  symptoms 
the  following  are  of  importance : — 

1.  The  area  of  cardiac  dullness  will  diminish  in  size  as  the 
strength  of  the  heart  fails.  In  even  a  moderately  severe 
case  of  this  type  the  absolute  cardiac  dullness  may  be  almost 
or  entirely  absent  and  the  relative  dullness  markedly  lessened 
in  size. 

In  severe  cases  of  cardiac  weakness  it  is  by  no  means 
unusual  to  find  that  even  the  relative  cardiac  dullness  is 
almost  or  entirely  absent  when  the  patient  is  lying  back  in 
bed,  and  these  cases  can  assume  no  other  attitude  owing  to 
extreme  weakness  and  the  tendency  to  fainting. 

In  such  a  case,  the  full  lung  resonance  will  come  down 
to  the  full  gastric  resonance,  in  and  internal  to  the  left  nipple 
line  (for  in  such  a  case  as  this,  the  dullness  of  the  left  lobe  of  the 
liver  will  also  be  entirely  absent  {ride  p.  68,  and  figs.  16-41). 

The  first  comment  that  will  be  made  upon  this  statement 
will  be  that  for  some  cause  or  other  the  lungs  are  unduly 
large  and  cover  up  the  heart.  Examination  of  the  size  of 
the  lungs  will  disprove  this  alternative,  for  percussion  of  the 
lower  limits  of  the  lung  resonance  show  that  the  diaphragm 
is  above  the  normal  level,  and  its  rise  shows  that  there  must 
be  a  distinct  lessening  of  the  total  volume  of  the  lungs  {vide  p.  68), 


WITH  SMALL  HEART  57 

and  therefore  the  disappearance  of  the  cardiac  dullness  must 
be  due  to  a  diminution  in  the  size  of  the  heart  or  a  falling  back- 
ward of  the  organ  into  the  chest.  Probably  both  causes  are 
at  work,  for  the  underfilled  organ  might  be  expected  to  fall 
somewhat  back  into  the  chest  under  the  action  of  gi-avity 
when  the  patient  is  lying  back  in  bed. 

I  have  not  taken  the  circumference  of  the  chest  in  these 
cases  nor  measured  the  angles  formed  by  the  ribs  in  order  to 
obtain,  if  possible,  further  confirmation  of  the  diminished  con- 
tent of  the  thorax ;  but  it  is  quite  probable  that  such  observations 
would  only  give  a  negative  result,  the  configuration  of  the 
chest  wall  being  normal  because  of  the  compensatory  change 
being  one  involving  the  diaphragm  only. 

2.  The  clinical  evidences  of  a  rise  in  the  average  level 
of  the  diaphragm  constitute  another  series  of  signs  of  cardiac 
failure  of  this  type. 

A  rise  in  the  level  of  the  gastric  resonance  is  one  of  the 
most  important  and  most  often  observed  of  these.  In  a 
shrinkage  of  the  thoracic  contents,  including  the  heart, 
the  left  half  of  the  diaphragm  would  naturally  rise  sooner 
than  the  right  half,  because  the  inertia  of  the  liver  would  tend 
to  retain  that  side  in  its  normal  situation.  The  gaseous 
contents  of  the  stomach  on  the  other  hand  would  have  no 
restraining  influence  upon  the  rise  of  the  left  half  of  the 
diaphragm  and  might  possibly  have  the  reverse  effect.  As 
this  question  of  the  rise  of  the  diaphragm  is  fully  discussed 
in  Essay  II,  at  p.  163,  nothing  more  need  be  said  here  except 
perhaps  that  the  rise  can  be  proved  to  be  due  to  a  lessening 
in  the  volume  of  the  intrathoracic  contents,  and  that  it  must 
be  due  to  a  lessened  fullness  of  the  heart  and  blood-vessels, 
especially  those  of  the  lungs. 

A  rise  in  the  upper  level  of  the  liver  dullness  on  the  right 
side  is  sometimes  of  value  as  indicating  a  rise  of  the  dia- 
phragm, in  spite  of  the  fact  that  it  is  less  marked  as  a  rule 
than  the  rise  in  the  gastric  resonance.  It  is  sometimes 
extreme  in  degree  {vide  p.  82,  and  fig.  49). 

3.  Emptiness  of  the  veins. 

In  cases  of  acute  heart  failure,  where  the  heart  muscle  is 
not  extremely  weak,  we  are  accustomed  to  look  for  the  fullness 


58  HEAKT  FAILURE 

of  the  veins  of  the  neck,  which  results  from  tricuspid  incom- 
petence, and  when  in  such  cases  it  is  absent  we  look  confidently 
for  the  dilatation  of  the  liver,  which  results  from  undue  fullness 
of  the  infeiior  vena  cava. 

Where,  however,  the  heart  muscle  is  extremely  weak,  the 
reverse  is  the  case ;  for  the  veins  of  the  neck  are  empty, 
and  the  supraclavicular  fossge  deeper  than  normal,  and  there 
is  no  sign  of  any  distension  of  the  liver,  but  rather  the 
reverse. 

4.  Another  sign  of  heart  failure  which  is  of  value  in 
measuring  the  muscular  strength  of  the  heart  is  the  size  of 
the  liver  dullness  as  judged  by  percussion  when  the  patient  is 
recumbent. 

In  muscular  failure  of  the  heart  there  is  diminution  of 
the  area  of  liver  dullness,  and  in  cases  of  extreme  heart  failure 
this  may  be  so  marked  that  there  is  almost  no  absolute  liver 
dullness  anteriorly  when  the  patient  is  lying  back,  and  it  is 
not  at  all  infrequent  to  find  that  there  is  no  absolute  liver 
dullness  anterior  to  the  right  nipple  line,  and  that  in  front  of 
this  line  the  gastric  or  intestinal  resonance  meets  the  resonance 
due  to  the  lung  with  no  intervening  absolutely  dull  area  such 
as  is  found  in  the  normal  chest. 

This  absence  of  dullness  is  due  in  part  to  diminution  in 
the  size  of  liver,  from  its  vessels  being  underfilled  with  blood, 
and  in  part  to  a  want  of  rigidity  due  to  the  same  cause  which 
allows  it  to  fall  away  from  the  chest  wall,  and  in  part  to 
altered  conductivity  to  percussion  vibrations.  This  condition 
of  the  liver  is  also  found  when  the  blood  volume  is  diminished 
from  causes  other  than  heart  failure,  and  is  fully  discussed 
at  p.  202. 

Some  of  these  phenomena  must  now  be  discussed  more 
in  detail. 

Changes  in  the  Pui.se  in  heart  weakness. — Changes 
in  the  pulse  may  be  indicative  of  the  onset  of  extreme 
muscular  failure  of  the  heart. 

One  of  the  most  important  changes  indicative  of  weakening 
of  the  heart  muscle  is  the  often  described  sudden  drop  in  the 
strength  and  volume  of  the  pulse  wave.     This  weakening  of 


WITH  SMALL  HEART  59 

the  pulse — ^in  an  attack  of  rheumatism,  for  instance — suggests 
inflammatory  damage  of  the  heart  by  peri-  or  myo- carditis. 
So  far  as  the  rate  is  concerned  a  sudden  slowing  of  the  pulse 
is  very  suggestive  of  toxic  poisoning  of  the  heart  muscle  in 
cases  where  the  patient  is  suffering  from  some  infective 
complaint  such  as  influenza.  Increase  in  the  rapidity  is 
not  so  sure  an  indication. 

A  more  important  sign  and  one  which  points  strongly  to 
myocardial  weakness  is  a  rise  in  the  tension  of  the  arterial  wall 
(as  measured  by  the  fullness  of  the  pulse  between  the  beats), 
associated  with  marked  feebleness  of  the  pulse  and  lowness  of 
the  blood  pressure — i.e.,  a  weak  pulse  of  relatively  high  tension. 
In  such  a  pulse  as  this  the  artery  remains  quite  full  between 
the  beats  and,  if  gentle  enough  pressure  be  used,  can  be  rolled 
under  the  finger  as  a  continuous  soft  cord  and  does  not  subside 
as  a  normal  pulse  does. 

The  contracted  state  of  the  arterioles  which  this  type  of 
pulse  implies  is,  in  all  ])robability  a  compensatory  phenomenon. 
The  heart  is  too  feeble  to  keep  much  blood  in  circulation, 
or  to  maintain  it  at  anywhere  near  the  normal  pressure,  and 
therefore  the  systemic  arterioles  are  kept  in  the  gi'eatest 
degree  of  contraction  that  the  weakened  heart  can  stand. 

This  serves  the  double  purpose  of  diverting  a  maximal 
amount  of  blood  from  the  systemic  circulation  to  the  brain 
and  heart  and  also  of  maintaining  the  blood  pressure  at  the 
highest  possible  level  throughout  the  whole  of  the  diastole, 
thus  enhancing  as  much  as  possible  the  effect  of  the  feeble 
systolic  rise  in  the  blood  pressure. 

In  enteric  fever  this  pulse  of  low  blood  pressure  with 
relatively  high  arterial  tension  can  very  frequently  be  noticed, 
and  it  speaks  cf  the  degree  to  which  the  heart  muscle  has 
been  weakened  by  the  action  of  the  specific  toxin. 

Such  a  pulse  as  this  will  suggest  caution  in  the  use  of  cardiac 
stimulants.  Flogging  an  exhausted  horse  may  result  in  his 
falling  dead  on  the  road. 

Changes  in  Heart  Sounds,  &c. — Diminution  in  the 
loudness  of  the  heart  sounds  is  a  valuable  indication  of  weaken- 
ing of  the  heart's  action,  and  is  always  present  in  muscular 


60  HEART  FAILURE 

failure.  The  marked  weakening  of  the  first  sound  of  the  heart 
which  is  so  characteristic  of  severe  enteric  fever  is  a  well-known 
indication  that  the  heart  muscle  is  being  damaged  by  the 
enteric  toxin. 

Sometimes  when  one  ventricle  is  more  involved  than  the 
other  in  a  case  of  fatty  degeneration,  the  relative  weakness 
of  the  sounds  on  that  side  of  the  heart  is  a  useful  guide. 

I  have  more  than  once  known  marked  weakness  of  the  right 
ventricular  sounds  confirm  the  diagnosis  of  fatty  degeneration 
mainly  limited  to  the  right  ventricle,  in  cases  of  marked  breath- 
lessness  combined  with  a  good  pulse  and  good  left  ventricular 
heart  sounds. 

Diminution  of  the  area  of  cardiac  dullness,  especially  if 
accompanied  by  weakening  of  the  cardiac  impulse,  is  an 
important  sign  of  weakness  of  the  heart  muscle. 

The  diminution  takes  place  on  all  sides  of  the  cardiac  area. 
The  heart  presumably  shrinks  in  volume,  and  so  the  lungs 
encroach  upon  it.  Instead  of  its  normal  shape  the  cardiac 
dullness  assumes  a  semi-ovoid  shape,  and  its  lower  border 
rises  above  the  normal  level :  for  the  lower  edge  of  the 
cardiac  dullness  is  encroached  upon  by  the  rise  in  the  gastric 
resonance  which  is  found  in  such  cases. 

The  cardiac  dullness  does  not  as  a  rule  reach  to  the  sternum 
unless  it  be  for  half  an  inch  or  so  at  its  lowest  part.  This 
change  in  the  area  of  the  cardiac  dullness  is  w'ell  shown  in 
figs.  41-51. 

Reference  to  p.  202  will,  however,  show  that  diminution 
in  the  area  of  the  cardiac  dullness  accompanied  by  a  rise  in 
the  diaphragm  may  be  due  to  causes  other  than  muscular 
failure  of  the  heart,  and  therefore  this  sign  cannot  be  taken 
by  itself  as  a  sign  of  heart  failure.  The  sudden  onset,  how- 
ever, of  such  a  diminution,  in  a  case  where  sudden  loss  of 
blood  or  malnutrition  could  be  excluded,  would  suggest  the 
occurrence  of  muscular  weakness  of  the  heart. 

Other  signs  of  cardiac  weakness. — The  remaining  signs 
of  weak  heart  muscle — namely,  the  rise  in  the  gastric  reson- 
ance and  rise  in  the  upper  level  of  the  liver  which  result 


WITH  SMALL  HEART  61 

from  a  rise  in  the  level  of  the  diaphragm,  and  also  the  diminution 
of  the  area  of  the  Uver  dullness,  are  dealt  with  in  Essays  II 
and  III.  They  are  signs  of  lessened  blood  supply,  and  are 
also  met  with  in  cases  of  haemorrhage  or  shrinkage  in  the 
volume  of  the  chculating  blood  from  other  causes,  and  are 
therefore  not  pathognomonic  of  myocardial  weakness. 

Emptiness  of  the  veins  of  the  neck  is  an  easily  observed 
sign,  and  its  presence  is  often  of  considerable  value  in  deciding 
whether  there  is  myocardial  weakness  or  not.  It  must  never 
be  forgotten,  however,  that  in  ordinary  heart  failure  in  valvular 
disease  the  veins  of  the  neck  may  be  relatively  empty,  in  spite 
of  the  presence  of  tricuspid  regurgitation,  where  the  Eustachian 
valve  has  given  way  and  the  blood  which  regm-gitates  from 
the  right  ventricle  passes  down  the  inferior  vena  cava  into  the 
liver,  instead  of  into  the  neck  veins.  A  very  cm'sory  examina- 
tion of  the  liver  will  sufi&ce  to  show  whether  the  emptiness  of 
the  neck  veins  be  due  to  this  cause  or  not. 

Eight  Ventkicle  in  muscular  weakness. — Before  leaving 
the  consideration  of  cardiac  failm-e  with  small  heart,  the 
question  may  be  asked :  Does  compensatory  diminution  in 
the  size  of  the  ventricle  occur  on  the  right  side  of  the  heart 
as  a  primary  phenomenon  ? 

As  a  secondary  phenomenon  it  must  occm-,  for  the  right 
side  of  the  heart  is  fed  by  the  left. 

All  the  evidence  points  against  the  right  ventricle  ever 
diminishing  in  volume  owing  to  a  primary  failure  in  its  muscular 
power. 

The  right  side  of  the  heart  is  more  dilatable  than  the 
left,  and  dilatation  leads  to  escape  of  the  blood  out  of  the  heart 
altogether  into  the  veins  and  not  simply  into  the  auricle  and 
the  closed  pulmonary  veins,  from  whence  it  is  certain  to  re-enter 
the  ventricle  during  its  next  expansion  phase,  as  is  the  case 
with  the  left  side  of  the  heart. 

A  primary  compensatory  diminution  in  the  size  of  the 
right  ventricle  is  not  therefore  necessary,  because  of  the  ease 
with  which  blood  escapes  from  an  embarrassed  right  ventricle. 

Under   certain  pathological    conditions    this    safety-valve 


62  HEART  FAILURE 

action  of  the  tricuspid  mechanism  is  largely  in  abeyance  ;  but 
under  these  circumstances  sudden  death  is  apt  to  occur  when 
there  is  over-distension  of  the  ventricle,  and  I  have  not  yet  been 
able  to  detect  any  sign  of  compensatory  diminution  in  the 
circulation  similar  to  that  which  occurs  in  weakness  of  the  left 
side  of  the  heart. 

The  cases  referred  to  are  those  where  the  distensibility  of 
the  right  side  of  the  heart  is  lessened  by  pericardial  adhesions, 
and  also  more  especially  by  adhesions  of  the  visceral  pleura 
to  the  sternum  and  ribs,  anteriorly,  as  well  as  over  the  vertebrse 
posteriorly.  This  adhesion  of  the  pleura  anteriorly  and 
posteriorly  forms  an  inelastic  tibrous  wall  to  the  right  of  the 
heart.  This  type  of  pleural  adhesion  is  frequently  the  cause 
of  sudden  death  under  chloroform  anaesthesia. 

As  a  rule,  however,  the  right  ventricle  is  not  faced  with  the 
risk  of  asystole,  like  the  left  ventricle,  owing  to  the  free  leakage 
through  the  tricuspid  valve,  and  the  distensibility  of  the  right 
auricle  and  great  veins.  In  cases  of  fatty  degeneration,  limited 
more  or  less  to  the  right  side  of  the  heart,  the  symptoms  are 
not  those  dealt  with  in  this  essay. 

The  appearance  of  the  above  phenomena  must  therefore  be 
looked  for  in  a  case  where  acute  myocardial  failure  is  to  be 
anticipated,  but  more  especially  the  signs  concerning  the  pulse, 
the  size  of  the  heart  and  strength  of  its  impulse,  the  size  of 
the  hepatic  dullness,  and  the  altered  level  of  the  gastric 
resonance. 

Diminution  in  the  Size  of  the  Heart  as  a  Sign  of 
Heart  Failure  in  Valvular  Disease,  &c. 

Before  leaving  the  subject  of  heart  failure  with  small 
heart  it  will  be  well  to  refer  to  the  phenomena  of  a  similar 
character  which  sometimes  occur  as  a  complication  of  valvular 
disease,  and  other  cases  of  cardiac  failure  with  which  dilatation 
is  associated. 

In  such  cases,  we  must  remember  that  acute  or  gradual  failure 
in  the  vitality  of  the  heart  muscle  may  be  associated  with 
a  (liminution  in  the  size  of  the  heart  and  liver.  Now,  considering 
that  dilatation  of  the  heart  and  enlargement  of  the  liver  are 


WITH  SMALL  HEART  63 

the  two  most  important  signs  of  heart  failure,  the  meaning 
of  such  a  diminution  may  be  mistaken,  and  the  mistake  may- 
prove  of  very  serious  import  to  the  patient.  Thus  in  a 
critical  case  of  heart  failure  with  dilated  heart,  I  have  noticed 
a  diminution  to  the  extent  of  over  an  inch  in  the  apparent 
size  of  the  greatly  enlarged  liver  taking  place  in  forty- eight 
hours.  This  was  no  case  of  improvement,  but  a  sign  of 
heart  failure  due  to  over-stimulation  ;  and  a  change  in  the  medi- 
cinal treatment  caused  a  return  of  the  liver  to  its  former  size 
in  another  forty-eight  hours,  together  with  signs  of  improved 
cardiac  action.  A  mistaken  interpretation  in  this  case  leading 
to  a  continuation  of  the  cardiac  stimulant  would  probably 
have  proved  most  disastrous  for  the  patient  (see  p.  201). 

A  similar  mistake  may  be  made  in  the  case  of  a  heart  which, 
owing  to  myocardial  weakness,  does  not  dilate  when  over- 
strained by  such  a  condition  as  acute  pneumonia.  A  normal 
or  a  small  heart  under  such  circumstances  may  be  a  sign  of 
dangerous  heart  failure. 

Dilatation  of  a  Weak  Heart  a  Sign  of   Eeturning 
Strength 

We  have  just  been  drawing  attention  to  the  fact  that 
diminution  in  the  size  of  the  heart  and  liver  may  in  exceptional 
cases  have  an  opposite  interpretation  to  that  which  it  usually 
bears. 

In  a  similar  way,  dilatation  of  the  heart  may  not  in- 
frequently have  to  bear  an  explanation  the  reverse  of  that 
which  is  usually  applicable  to  it ;  for  in  the  case  of  small 
heart,  due  to  myocardial  weakness  (of  which  we  have  been 
speaking),  one  of  the  early  signs  of  returning  vigour  may 
not  only  be  a  return  to  its  normal  size,  but  also  an  actual 
dilatation. 

Such  a  dilatation  must  be  looked  upon  as  a  satisfactory 
sign  in  such  a  case  {vide  p.  195,  and  figs.  42-52). 

As  an  illustration  of  the  way  in  which  the  progress  of  a 
weak  heart  may  be  observed  by  recourse  to  these  methods 
of  physical  examination,  I  would  refer  to  the  series  of  diagrams 
given  on  pp.  66  and  100,  and  also  to  Plate  I. 


64  HEART  FAILURE 

The  following  case  is  of  great  interest  in  this  connection, 
for  its  shows  very  well  how  the  principles  of  diagnosis  here 
laid  down  are  of  service  in  clearing  up  a  somewhat  difficult 
case  of  heart  failure. 

The  patient,  a  man  of  about  forty  years  of  age,  had  an 
attack  of  rheumatic  fever  eight  months  prior  to  my  seeing  him, 
and  ever  since  had  suffered  from  dyspnoea  with  occasionally 
some  dropsy  of  liis  ankles.  His  breathlessness  was  considerable, 
for  he  could  only  walk  up  some  five  or  six  steps  at  a  usual 
pace,  and  in  order  to  do  a  whole  flight,  he  would  have  to  go 
very  slowly.  The  man  was  rather  pale,  and  it  was  stated  that 
when  he  over-exerted  himself,  he  was  apt  to  go  very  pale.  On 
examination  it  was  found  that  the  veins  of  the  neck  were  quite 
empty  when  standing  up,  but  filled  up  slightly  when  he  lay 
down,  showing  some  false  pulsation,  but  no  signs  of  tricuspid 
regurgitation.  The  hver  dullness  to  the  right  was  practically 
normal,  and  also  showed  no  signs  of  regurgitation  into  the 
inferior  vena  cava.  The  pulsation  in  the  jugular  bulb  was 
about  normal  m  volume  and  of  fair  strength.  The  heart  itself 
was  not  enlarged  and  was  apparently  smaller  than  normal, 
for,  although  the  apex  could  be  just  felt  in  about  the  nipple 
line  in  the  fifth  interspace  when  he  was  standing  up,  when 
he  lay  down  there  was  well-marked  gastric  resonance  in  the 
fifth  space  as  far  as  the  nipple  line,  and  there  was  very  little, 
if  any,  pulsation  to  be  felt.  There  was  no  absolute  cardiac 
dullness,  and  the  relative  dullness  was  only  to  be  fovmd  in 
the  fourth,  and  for  about  the  normal  extent  in  the  third,  inter- 
space. The  sternum  was  resonant,  and  the  dullness  of  the  left 
lobe  of  the  liver  was  absent.  As  regards  the  heart  sounds 
there  was  at  the  apex  a  well-marked  mitral  systohc  murmur 
accompanying  a  short  and  not  very  loud  first  sound.  The 
second  sound  was  also  rather  short  and  sharp.  On  listening 
over  the  right  ventricle  it  was  found  that  there  was  no  evidence 
of  marked  overaction  as  would  have  been  expected  considermg 
his  breathlessness  and  the  presence  of  evident  mitral  regurgi- 
tation. The  sounds  were  of  only  moderate  loudness,  and  no 
pulsation  could  be  felt.'  The  pulse  was  of  moderate  volume 
and  strength  and  was  markedly  irregular.  The  cardiac  irregu- 
larity was  of  the  type  that  we  now  associate  with  auricular 
fibrillation. 


PLATE  T 


A  Photogkaph  of  the  Chest,  showing  the  rapid  return  of  the  Heart  and 
Liver  Dullness  towards  Normal  after  a  diminution  in  size  due  to 
Cardiac  Weakness. 

The  results  of  percussion  on  November  7,  1l',  and  14,  1911,  are  here  shown.  The  ribs  are  marked  in 
roman  nimierals,  and  the  costal  arch  (O.A.)  by  a  broken  line.  The  outline  o£  the  organs  on  the  7th  is 
shown  by  a  continuous  line,  on  the  12th  by  a  broken  line,  and  on  the  14th  by  a  dotted  line.  For  the  sake 
of  clearness,  shading  has  been  added — consisting  of  vertical  lines  over  the  cardiac  and  liver  areas  as  they 
were  on  the  7th,  obhque  lines  for  the  12th,  and  dotted  shading  for  the  14th.  t^hort  dark  lines  are  used  for 
the  absolute  dullness  on  November  14,  and  only  the  anterior  part  of  the  absolute  liver  dulhiass  is  shaded. 
Note  the  reappearance  of  the  absolute  cardiac  dullness  and  of  the  relative  dullness  of  the  left  lobe  of  the 
liver  on  November  14,  although  the  gastric  resonance  was  still  obtainable  in  the  fourth  interspace.  Note 
also  the  upward  dilatation  of  the  heart  into  the  second  interspace  on  the  14th,  although  the  patient  was 
still  confined  to  bed. 


WITH  SMALL  HEART  65 

The  diagnosis  here  was  mitral  incompetence,  with  consider- 
able myocardial  weakness  and  also  auricular  fibrillation  (see 
fig.  1). 

The  diagnosis  depended  upon  the  fact  that,  in  spite  of 
the  mitral  regurgitation  and  breathlessness,  there  was  no 
dilatation  or  hypertrophy,  the  heart  being,  on  the  contrary, 
smaller  than  normal,  as  was  shown  by  the  high  left  diaphragm 
and  the  lessened  area  of  cardiac  dullness ;  nor,  in  spite  of  the 
faulty  action  of  the  left  ventricle,  was  there  any  compensatory 
overaction  of  the  right  ventricle.  Another  evidence  of  weak 
muscular  action  was  the  fact  that,  in  spite  of  the  cardiac 
failure  and  breathlessness,  there  was  no  over-distension  of 
the  vems,  and  the  dyspnoea  was  accompanied  by  pallor  rather 
than  by  cyanosis  when  he  over-exerted  himself. 

In  this  case,  then,  the  rheumatic  fever  appeared  to  have  done 
more  damage  to  the  heart  wall  than  to  the  valves  (although 
there  was  some  mitral  incompetence),  and  the  damage  to  the 
heart  waU  seemed  also  to  have  caused  amicular  fibrillation. 
So  far  as  the  question  of  rigidity  of  the  heart  wall  was 
concerned,  it  was  only  possible  to  say  that  there  was  no  evidence 
of  any  abnormal  rigidity,  and  that  the  diminution  in  the  size 
of  the  heart  pointed  to  there  being  none.  The  absence  of 
dilatation  was  sufiiciently  explained  by  the  amount  of 
muscular  weakness  present. 

The  above  estimate  of  the  patient's  condition,  which  was 
made  at  his  first  visit  on  August  21, 1913,  was  confirmed  by  the 
after-history  of  the  case,  which  was,  shortly,  as  foUows : — 

He  was  seen  a  second  time,  on  September  11,  and  it  was 
found  that  the  heart  was  larger  (as  showTi  in  fig.  2),  and  the 
diaphragm  lower.  The  apex  was  now  4|  inches  from  the 
sternum  in  the  fifth  interspace,  instead  of  being  in  the  fourth 
interspace  and  under  3  inches  from  the  sternum.  The  patient 
stated  that  he  was  stronger  and  less  breathless  on  exertion. 
The  heart,  though  still  irregular  enough  to  suggest  auricular 
fibrillation,  was  stronger,  and  its  sounds  much  louder.  The 
mitral  systoUc  murmur,  though  loud  when  recumbent,  was 
inaudible  when  the  patient  was  erect. 

In  October,  the  heart  was  decidedly  dilated,  with  3  inches 
of  relative  dullness  in  the  third  left  interspace,  and  31  inches  of 


A  Case  in  wmcn  thk  Occurrence  of  Gradual  Cardiac  Enlargement  Indicated 
Returning  Strength  after  Myocardial  Weakness 


-if recumbent 
■Ap€x5^A 
J f  erect 


Samuel  W.,  aged  tliirty-eight,  August  21, 
1913,  eight  months  after  rheumatic  fever. 
Mitral  regurgitation,  but  no  dilatation  or 
venous  plethora  because  of  myocardial  weak- 
ness. On  stairs  can  only  do  sis  or  seven 
steps  at  ordinary  pace. 


Fig.  2. 

Samuel  W.,  September  11,  1913.  Heart 
larger.  Sounds  louder.  Impulse  more 
forcible.  Patient  less  breathless.  Can  now 
mount  eighteen  or  twenty  steps  at  ordinary 
pace.  The  amount  of  relative  cardiac  dull- 
ness to  the  left  of  the  sternum  is  marked  on 
the  diagram. 


^S.=5^) 


Fig.  3. 

Samuel  W.,  October  2,  1913.  Heart  now 
considerably  dilated,  but  patient  still 
improving,  and  less  breathless.  (Mitral 
systolic  murmur  now  loud  and  audible  to 
axilla.) 


■tA=6" 


Fig.  4. 

Samuel  W.,  November  13,  1913.  Heart 
now  greatly  dilated  (see  measurements  on 
diagram),  but  its  action  is  more  vigorous 
than  a  month  ago  ;  and  the  patient  says  he 
feels  stronger,  and  can  walk  three  miles  of 
rather  hiUy  road  in  fifty-five  minutes. 


WITH  SMALL  HEART 


67 


absolute  dullness  in  the  fourth  space,  and  an  apex  beat  5|  inches 
from  the  sternum.  The  patient  was  very  much  stronger,  and 
could  walk  two  miles  on  the  level  in  an  hour  without  undue 
breathlessness,  but  was  cautioned  not  to  do  so.  The  mitral 
systolic  murmur  was  loud  and  'audible  into  the  axilla 
(see  fig.  3). 

In  November,  when  seen  again,  the  patient  stated  that 
he  was  stronger  and  better  than  at  the  last  visit ;  but  the 
heart  was  still  more  dilated,  and  the  apex  was  6  inches  from 
the  sternum,  nearly  in 
the  anterior  axillary  hne, 
and  there  was  nearly  5 
inches  of  absolute  dull- 
ness in  the  fourth  inter- 
space. There  were  now 
4|  inches  of  relative  dull- 
ness in  the  third  left 
interspace,  but  no  evi- 
dence of  dilatation  to  the 
right.  The  heart  sounds 
were  now  of  good  loud- 
ness, and  there  was  a 
short  rough  systolic  mur- 
mur at  the  apex,  but  no 
auscultatory  signs  of 
overaction  of  the  right 
ventricle  (see  fig.  4).  He 
could  now  walk  three 
miles  of  rather  hilly  road 

in  fifty-five  minutes  with  only  a  little  breathlessness  on  the 
last  hill — which  was  not  a  steep  one. 

At  the  next  visit  the  increased  strength  of  the  heart  began 
to  show  itself  for  the  first  time  by  lessened  instead  of  by  in- 
creasing dilatation.  The  dullness  in  the  third  interspace  was 
about  the  same,  but  in  the  fourth  and  fifth  it  was  about  |  inch 
less. 

The  occurrence  of  dilatation  here  as  the  heart  gained 
strength  showed  its  distensibility,  and  also  that  the  heart 
muscle  had  been  so  weakened  by  the  rheumatism  eight  months 
earlier  that  the  thinner  part  of  the  ventricle  walls  gave  way 
as  soon  as  the  heart  muscle  was  strong  enough  to  develop  an 
approximately  normal  amount  of  mtraventricular  pressure. 

f2 


Fig.  5. 

Samuel  W.,  December  18,  1913.  Dilatation  now 
beginning  to  lessen  (apex  half  an  inch  nearer  the 
sternum).     Patient  continues  to  improve. 


68  HEART  FAILURE 

In  such  a  case  the  reappearance  of  the  cardiac  dullness, 
coupled  with  increase  in  the  loudness  of  the  heart  sounds 
and  the  reappearance  of  the  cardiac  impulse,  can  be  taken 
as  proof  that  the  strength  of  the  heart  is  returning.  This 
proof  is  often  of  considerable  clinical  value,  for  where  such 
a  patient  is  of  a  nervous  temperament,  the  first  few  times  of 
getting  out  of  bed  often  bring  about  a  sense  of  either  weakness, 
faintness,  or  actual  palpitation.  This  is  apt  to  cause  alarm 
to  the  patients  and  their  friends ;  but  I  have  found  that  such 
symptoms  can  often  be  ignored  if  the  heart  be  carefully  watched, 
and  that  they  are  of  the  nature  of  a  habit  weakness,  and  will 
pass  off  if  the  exercise  be  persevered  with.  Sometimes  it 
has  been  necessary  almost  to  coni'pel  the  patient  to  attempt 
mild  forms  of  exercise,  because  of  his  fear  that  the  discomfort 
and  faintness  it  induced  was  the  same  as  that  which  character- 
ised his  attack  of  true  myocardial  weakness  and  which  did 
result  in  actual  fainting.  In  such  cases,  where  the  physical 
signs  show  that  the  heart  is  not  really  being  injured  by  the 
exertion,  a  change  of  air  and  scene  will  often  speedily  restore 
and  reassure  the  patient.  The  following  case  illustrates  this 
point  :  it  is  also  referred  to  at  p.  118,  where  diagrams  of  the 
chest  are  also  given : — 

Dr.  G.,  aged  twenty-six,  had  had  an  attack  of  diphtheria  six 
weeks  ago.  There  had  been  no  paralysis,  but  the  patient  had 
had  troublesome  heart  attacks  ever  since  and  had  been  confined 
to  bed.  The  attack  consisted  of  intermission  of  the  pulse 
with  a  sense  of  heart  weakness  and  faintness,  making  the 
patient  afraid  to  move. 

On  examining  her  it  was  found  that  the  pulse  was  small 
and  weak,  the  veins  of  the  neck  were  empty,  and  there  was 
no  evidence  of  any  venous  engorgement  of  the  Uver  :  on 
the  contrary,  all  signs  pointed  to  emptiness  of  the  heart  and 
veins. 

There  was  no  cardiac  impulse  to  be  seen  or  felt  anywhere, 
and  there  was  no  cardiac  dullness  to  be  detected,  for  the  full 
gastric  resonance  came  as  high  as  the  lower  border  of  the 
fourth  rib,  and  was  here  met  by  the  full  lung  resonance,  showing 
a  very  high  diaphragm.  The  hver  dullness,  too,  was  much 
smaller  than  normal.  The  heart  sounds  were  free  from  mur- 
murs, but  were  very  weak  and  wanting  in  vigour.     A  fortnight 


WITH  SMALL  HEART  69 

later,  it  was  found  that  there  were  some  signs  that  the  heart 
was  stronger.  There  was  a  trace  of  relative  cardiac  dullness 
in  the  fourth  interspace  internal  to  the  nipple  line,  though  there 
was  still  some  gastric  resonance  in  this  same  interspace  ; 
there  was  also  a  trace  of  cardiac  pulsation  to  be  detected  here. 
On  auscultation,  there  was  more  vigour  about  the  heart  sounds  : 
they  were  not  quite  so  weak  and  short,  the  second  sound  was 
moderately  loud  at  the  apex,  and  there  was  a  faint  systohc 
murmur  over  the  right  ventricle  in  the  fourth  interspace  near 
the  sternum.  The  liver  dullness  was  small.  Its  absolute 
dullness  began  about  the  normal  level  in  the  sixth  interspace, 
but  it  did  not  reach  to  within  1|  inch  of  the  costal  arch,  nor 
did  it  come  internal  to  the  right  vertical  nipple  line.  The 
relative  Hver  dullness  began  above  at  about  the  normal  level, 
but  did  not  quite  reach  down  to  the  costal  arch,  and  there  was 
only  a  trace  of  Hver  dullness  in  the  middle  line  at  the  base  of 
the  sternum  {vide  figs.  16,  17,  18;  and  118). 

The  patient  progressed  very  slowly ;  but  when  seen  two 
weeks  later,  there  was  well-marked  cardiac  pulsation  in  the 
fourth  interspace,  and  a  trace  of  pulsation  in  the  third,  and 
the  apex  was  under  the  fifth  rib  and  was  just  to  be  felt  in  the 
upper  part  of  the  fifth  interspace  in  the  nipple  line. 

At  the  sternal  end  of  the  fourth  interspace,  the  cardiac 
dullness  was  nearly  absolute. 

The  liver  dullness  had  not  increased  in  size,  but  was,  in 
fact,  a  trifle  less  ;  for  its  absolute  dullness  did  not  reach  to 
within  2  inches  of  the  costal  arch. 

After  another  week  or  two,  as  the  heart  continued  to  gain 
strength,  the  patient  was  allowed  out  of  bed  ;  but  after  getting 
up  a  few  times,  the  question  arose  as  to  the  wisdom  of  doing 
so,  for  it  not  only  produced  a  feehng  of  faintness  and  exhaustion, 
but  also  a  certain  amount  of  palpitation  which  somewhat 
alarmed  the  patient.  However,  a  careful  examination  of  the 
heart  showed  that  it  was  evidently  stronger,  the  sounds  were 
louder,  and  there  were  no  signs  of  any  dilatation,  and  the  patient 
was  advised  to  continue  to  get  up  and  take  a  gradually  in- 
creasing amount  of  exercise.  The  result  was  entirely  satis- 
factory. This  case  is  again  referred  to,  in  connection  with 
palpitation  as  a  cardiac  habit,  at  p.  118,  and  figures  showing 
the  changes  in  the  size  of  the  heart  and  liver  are  there  given. 


70  HEART  FAILURE 


Early  Diagnosis  of    Heart  Failure  in   the  relatively 
EiGiD  Heart  of  Later  Life 

summary 

Introductory. 

(i)  Modifications  in  the  signs  and  symptoms  of  heart 
failure  which  result  from  the  increasing  rigidity  of 
the  fibrous  tissues  which  characterises  advancing  life. 

1.  As  regards  the  body  generally. 

2.  As  regards  the  heart  and  pericardium. 

(ii)  Modifications  in  the  signs  and  symptoms  of  heart 
failure  due  to  the  arterial  changes  of  later  life. 

1.  Rise  in  blood  pressure. 

2.  Disease  of  coronary  arteries. 

I.    DiSTENSIBILITY   OF    THE    HeART   IN    LaTER   LiFE. 

II.  Early  Diagnosis  of  Heart  Failure  with  Enlarge- 
ment in  Relatively  Rigid  Hearts. 
III.  Heart  Failure  without  Enlargement  in  Strong  or 
only  Moderately  Weak  Hearts  of  considerable 
Rigidity. 
IV.  Heart  Failure  without  Enlargement  in  decidedly 
Weak  and  Relatively  Rigid  Hearts. 
Symptoms  :     Dyspnoea,  faintness,  pain,  palpitation,  phy- 
sical signs. 
Illustrative  cases  of  cardiac  failure  in  weak  and  relatively 
rigid  hearts. 
V.  Early  Diagnosis  of  Muscular  Failure  of  the  Heart 

IN  Later  Life  in  Cases  of  Valvular  Disease. 
VI.  Short  Notes   upon   some   of   the   Diagnostic   Diffi- 
culties   which    Surround     the    Recognition    of 
Heart  Failure  in  Later  Life,  as  regards — 


IN  LATER  LIFE  71 

1.  Dyspnoea. 

2.  Palpitation. 

3.  Faintness. 

4.  Anginous  pain. 

5.  Venous  phenomena. 

6.  The  recognition  of  arterial  resistance  as  a  factor 

in  cardiac  failure. 

7.  The  recognition  of  rigidity  of  the   heart  wall 

as  a  factor  in  cardiac  failui'e. 

8.  Difficulties    in    connection    with    the    physical 

examination  of  the  heart. 

9.  Difficulties  due  to  one  ventricle  being  weak  while 

the  other  is  strong  (with  illustrative  cases). 
10.  Summary  of  various  types  of  difficulty. 

« 

INTRODUCTOBY 

This  section  on  the  early  diagnosis  of  heart  failure  in  later 
life  must  be  commenced  with  an  apology,  because  the  subject, 
in  the  present  imperfect  state  of  om-  knowledge,  is  a  very 
difficult  one  to  treat  concisely  and  with  scientific  method. 

The  fact  that  many  of  the  physical  evidences  of  heart 
failure,  upon  which  we  rely  for  purposes  of  diagnosis  in  early 
life,  are  less  marked  or  absent  in  later  life,  and  that  we  often 
have  to  diagnose  heart  failm-e  because  of  the  absence  of  such 
physical  signs,  does  not  help  to  make  the  subject  an  easy 
one  to  deal  with.  Again,  in  later  life  many  of  the  evidences 
of  heart  failure  are  capable  of  bearing  exactly  opposite  inter- 
pretations. For  instance,  fullness  of  the  veins  of  the  neck 
may  be  a  sign  of  the  failm-e  of  a  moderately  strong  heart,  or 
its  appearance  may  be  the  sign  that  a  weak  heart  is  gaining 
strength.  Again,  a  lessening  in  the  degree  of  fullness  of  the 
neck  veins  may  be  the  sign  that  a  strong  heart  is  gaining 
strength,  or  that  a  weak  heart  is  losing  strength  {vide  p.  105 
below).  Diminution  in  the  size  of  the  right  ventricle  may 
mean  return  of  strength  in  a  moderately  strong  heart,  or 
dangerous  weakness  in  a  weak  heart.  Again,  another  difficulty 
which  has  to  be  faced  is  that  the  absence  of  well-marked  sigjis 
in  later  hfe  necessitates  a  far  greater  rehance  upon  sym'ptoms 


72  HEART  FAILURE 

for  the  diagnosis  of  heart  failure  :  and  symptons  are — especially 
in  adult  and  later  life — very  unreliable,  because  of  the  frequency 
with  which  symptoms  of  true  cardiac  failure  are  simulated  by 
symptoms  which  arise  merely  from  reflex  disturbances,  and 
vice  versa. 

In  order  to  try  to  bring  some  method  into  the  treatment 
of  this  complex  subject,  it  is  proposed  first  to  discuss  the  main 
differences  between  the  heart  in  later  and  early  life  and  the 
main  points  upon  which  reliance  can  be  placed,  and  then  to  take 
up  the  diagnostic  difficulties  in  connection  with  the  symptoms 
and  signs  of  heart  failure,  illustrating  the  various  points  by 
giving  actual  clinical  cases. 

In  summarising  the  various  points  upon  which  we  have 
to  rely  for  the  early  diagnosis  of  heart  failm-e  in  later  life,  we 
find  that  there  are  distinct  differences  as  compared  with  those 
already  described  as  characterising  heart  failure  in  early  life, 
and  the  differences  depend  mainly  upon  two  characteristics 
of  mature  and  later  years — namely  : — 

1.  The  tendency  which  the  fibrous  tissues  of  the  body 
generally  have  to  consolidate  and  become  more  rigid  as  life 
advances,  and  thus  to  modify  the  signs  and  symptoms  of  heart 
failure  ;  and 

2.  The  tendency  to  abnormalities  of  the  arteries,  either  of 
the  nature  of  spasmodic  contraction  and  rigidity — such  as 
is  associated  with  faulty  ehmination  of  waste  products — or 
abnormalities  due  to  degenerative  changes  in  them. 

To  take  up  the  first  group. 

I.  Changes  Due  to  Increased  Eigidity  of  Fibrous 
Tissues. — 1.  So  far  as  the  general  tissues  of  the  body  are  con- 
cerned, the  only  modifications  will  be  in  those  signs  of  heart 
failure  which  depend  upon  variation  in  the  position  or  size 
of  organs. 

Thus  it  is  not  to  be  expected  that  in  later  life  alterations 
in  the  volume  of  the  intrathoracic  contents  will  result  in 
alterations  in  the  level  of  the  diaphragm  as  readily  as  is  the 
case  when  the  fibrous  tissues  are  elastic,  earlier  in  life.  More 
especially  is  this  the  case  with  regard  to  the  right  half  of  the 
diaphragm,  and  in  later  life  it  is  not  usual  to  find  any  marked 


IN  LATER  LIFE  73 

rise  in  the  upper  level  of  the  liver  dullness  in  myocardial 
weakness,  however  severe. 

Eise  of  the  left  half  is,  however,  a  valuable  sign,  although 
it  be  less  extreme  than  earlier  in  life. 

So  far  as  alteration  in  the  size  of  the  Hver  dullness  is 
concerned,  the  more  rigid  tissues  of  later  life  will  not  show 
such  extreme  changes  when  the  organ  is  underfilled  with  blood 
as  was  the  case  earlier  in  life. 

2.  Changes  in  the  Heart  and  Pericardium. — The  chief 
bearings  of  these  changes  upon  the  early  diagnosis  of  heart 
failure  in  later  life  are  as  follows  : — 

(1)  Where  heart  failure  is  accompanied  by  enlargement, 
although  the  type  of  dilatation  will  be  the  same  as  that  occurring 
in  adult  life  (p.  31),  the  degree  of  enlargement  will  be 
less,  and  the  greater  the  rigidity  the  less  will  the  amount  of 
dilatation  be  for  any  given  amount  of  distensile  force. 

(2)  When  the  degree  of  rigidity  of  the  heart  is  very 
considerable  there  may  be  no  yielding  at  all  of  the  heart 
wall,  in  spite  of  the  heart  being  of  considerable  muscular 
strength. 

Take,  for  instance,  a  case  of  overstrain  in  a  heart  of  good 
muscular  strength  with  a  moderately  distensible  wall.  In 
this  case  the  rise  in  intraventricular  pressure  necessary  for 
the  carrying  on  of  the  circulation  may  be  in  excess  of  the 
resisting  power  of  the  heart  wall,  and  the  heart  then  dilates. 
Take,  however,  another  heart  of  the  same  muscular  strength 
and  facing  the  same  amount  of  overstrain,  but  in  which  the 
fibrous  rigidity  of  the  wall  is  so  great  that  it  can  withstand 
the  increased  intraventricular  pressure. 

Although  in  the  two  cases  the  heart  muscle  is  strained  to 
the  same  extent  by  meeting  the  increased  resistance  it  has 
to  face,  there  will,  in  the  one  case,  be  heart  failure  with  enlarge- 
ment, and  in  the  other,  heart  failure  without  enlargement. 

This  is  a  point  upon  which  stress  must  be  laid.  In  study- 
ing heart  failure  in  later  life,  the  muscular  strength  of  the 
heart  must  not  be  confused  with  the  fibrous  strength  of 
the  heart  wall,  and  the  two  must  be  considered  separately. 
A  heart  that  dilates  in  the  face  of  overstrain'^is,  in  later  life, 
often  stronger  muscularly  than  one  that  does  not  dilate. 


74  HEART  FAILURE 

Therefore,  in  later  life,  we  must  recognise  a  fresh  group — 
namely,  cases  where  there  is  heart  failure  without  enlargement 
in  moderately  strong  hearts. 

(3)  Eigidity  of  the  heart  wall  will  interfere  more  or  less 
completely  with  the  development  of  compensatory  diminution 
in  the  size  of  the  heart  in  extreme  myocardial  weakness. 

11.  Modifications  in  the  Signs  and  Symptoms  of  Heart 
Failure  due  to  the  arterial  changes  of  later  hfe. 

The  second  of  the  two  main  changes  that  we  have  spoken 
of  must  now  be  taken  up — namely,  the  changes  in  the  arteries. 

1.  EiSE  IN  Blood  Pressure  due  to  reflex  or  organic 
narrowing  of  the  peripheral  arteries. — The  diagnosis  of  early 
cardiac  failure  is  rendered  more  complicated  in  later  life  by 
the  greater  frequency  with  which  changes  in  the  blood  pressure 
occur,  for,  although  cases  showing  high  blood  pressure  are 
sometimes  found  in  adolescence  and  earlj'-  adult  life,  they  are 
by  no  means  common,  whereas  in  later  life  they  are  extremely 
frequent. 

Therefore,  in  an  adult,  in  estimating  the  amount  of  work 
the  heart  is  doing,  we  not  only  take  into  account  the  energy 
necessary  for  the  amount  of  exertion  the  patient  is  making, 
but  we  must  also  be  careful  to  estimate  as  nearly  as  possible 
the  extra  work  that  may  be  thrown  upon  the  heart  by  the 
interference  with  the  circulation  which  abnormal  rigidity  of 
the  smaller  arteries  brings  about.  The  uncertainties  which 
are  apt  to  make  this,  at  times,  far  from  easy  are  dealt  with 
later  on  when  considering  '  Diagnostic  Difficulties  in  Later 
Life.'  The  different  causes  of  high  blood  pressure  do  not 
come  within  the  scope  of  our  subject,  and  are,  moreover,  dealt 
with  fully  enough  in  medical  literature. 

Another  condition  which  may  greatly  complicate  the 
diagnosis  of  heart  failure  is  rigidity  of  the  first  part  of  the 
aorta  as  a  result  of  atheroma  or  of  a  more  rare  inflammatory 
affection — namely,  chronic  mediastinitis.  Considering  that 
the  first  part  of  the  aorta  (aided  by  the  elasticity  of  the  arteries) 
acts  as  an  expansion  chamber,  allowing  the  heart  to  keep  up 
a  continuous  flow  of  blood,  although  it  merely  gives  a  short 


IN  LATER  LIFE  75 

sharp  stroke,  interference  with  the  elasticity  of  this  portion 
of  the  aorta  Avill  necessitate  on  the  part  of  the  ventricle  a  long- 
sustained  contraction  in  order  properly  to  drive  the  blood 
into  the  peripheral  vessels,  and  this  may  readily  lead  to  cardiac 
failure.  Its  presence  may  cause  uncertainty  in  diagnosis,  for 
it  may  not  be  easy  to  understand  the  reason  for  a  strong 
sustained  pulse  in  a  dilated  and  hypertrophied  heart  with  no 
apparent  cause  for  failure. 

2.  Disease  Affecting  the  Coronary  Arteries. — The 
liabihty  of  the  heart  in  later  life  to  suffer  from  mahiutrition, 
owing  to  disease  of  the  coronary  arteries,  forms  one  of  the 
most  striking  difference?  between  heart  failure  in  early  and  in 
later  life,  and  greatly  adds  to  the  difficulty  in  recognising  cardiac 
failure.  When  speaking  of  the  cause  of  heart  failure  with 
small  heart  in  adolescence,  attention  was  drawn  to  the  fact 
that  the  main  agencies  which  produced  myocardial  weakness 
were  general  ones — such  as  the  toxaemia  of  influenza,  diphtheria, 
rheumatism,  etc.  These  agencies,  in  spite  of  the  fact  that 
there  may  be  small  localised  inflammatory  foci  in  the  heart 
muscles  (such  as  have  been  demonstrated  in  rheumatic  myo- 
cardial weakness  by  many  observers),  rarely,  if  ever,  seem  to 
involve  one  ventricle  more  than  the  other,  and  clinical 
symptoms  of  general  muscular  failure  therefore  result. 

When  dealing,  however,  with  the  adult  heart  the  commonest 
causes  of  muscular  weakness  are  circulatory  in  origin — due  to 
interference  with  the  cii-culation  in  the  coronary  arteries  by 
atheroma.  Under  such  cii'cumstances  it  is  by  no  means 
uncommon  for  the  arterial  supply  of  one  ventricle  to  be 
interfered  with  to  a  greater  extent  than  that  of  the  other. 

Therefore,  we  may  meet  with  hearts  where  one  ventricle  is 
moderately  strong,  while  the  other  one  is  very  weak ;  and  we 
may  occasionally  be  surprised  to  find  a  patient  dying  of  breath- 
lessness  of  cardiac  origin,  in  spite  of  the  fact  that  the  pulse 
is  fairly  good  and  strong;  for  this  is  what  occurs  where  the 
coronary  supply  to  the  right  heart  is  greatly  interfered  with, 
while  that  of  the  left  ventricle  is  fairly  good.  Such  a  case  is 
described  on  p.  154.  Wliere,  on  the  other  hand,  the  left 
ventricle  is  the  weaker,  the  diagnosis  may  be  more  easy  if 
fainting  or  marked  weakness  occm-;   but  it  may  be  quite  as 


76  DISTENSIBILITY  OF  THE  HEART 

difficult  as  in  the  case  of  the  right  ventricle — for  example,  in 
the  cases  where  a  patient  dies  suddenly  from  fatty  degeneration 
without  his  medical  attendant  being  aware  that  there  is  any 
dangerous  weakness  of  the  heart. 

This  subject  will  be  further  dealt  with  and  illustrative  cases 
given  in  the  Essay  on  'Diagnostic  Difficulties  in  the  Heart 
Failure  of  Later  Life.' 

DiSTENSIBILITY   OF    THE   HeART   IN    LaTER   LiFE 

The  distensibility  of  the  heart  in  later  life  must  now  be 
discussed  in  its  relation  to  the  early  diagnosis  of  cardiac  failure. 

The  amount  of  distensibiUty  possessed  by  the  heart  plays, 
in  later  life,  an  even  more  important  part  as  regards  the  diag- 
nosis and  prognosis  of  heart  failure  than  it  does  in  early  life ; 
but  its  amount  is  much  less  easily  ascertained,  and  for  this 
reason,  that,  in  adolescence,  owing  to  the  softness  of  its  tissues, 
the  heart  changes  its  form  and  size  easily,  giving  positive 
chnical  evidence  of  its  distensibility,  whereas  in  later  Hfe 
its  maturer  tissues  yield  much  less  easily,  and  thus  the  signs 
of  its  lessened  distensibility  are  mainly  negative. 

But  before  going  further  with  the  subject,  this  whole 
question  as  to  the  rigidity  of  the  fibrous  tissues  increasing 
with  advancing  age  must  be  discussed  in  a  little  more  detail, 
because  I  am  not  aware  that  it  is  accepted,  so  far  as  the  heart 
is  concerned,  as  a  proved  fact ;  and  the  anatomist  may  object 
that  there  is  not  enough  true  fibrous  tissue  in  the  heart  wall 
to  render  probable  such  a  change  as  that  here  suggested. 

Li  the  first  place,  this  proposition  as  to  an  increase  in  the 
rigidity  of  the  fibrous  tissues  is  certainly  accepted,  so  far  as 
the  tissues  of  the  body  generally  are  concerned,  and  it  will 
not  be  disputed  that  one  of  the  main  differences  between 
early  and  later  hfe  hes  in  the  condition  of  the  fibrous  tissues, 
which  in  early  life  are  relatively  soft  and  distensible. 

The  body  is,  to  use  a  famUiar  phrase,  more  supple  in  early 
life.  With  advancing  years,  the  tendency  of  the  fibrous  tissues 
is  to  become  less  and  less  distensible,  the  joints  get  stiffer  and 
less  easily  adaptable  to  altered  uses — such  as  the  learning  of 
new  gymnastic  exercises,  &c.    Dislocation  of  the  joints,  too,  is 


IN  LATER  LIFE  77 

less  likely  to  occur  than  in  early  life,  owing  to  the  greater 
rigidity  of  their  fibrous  supports.  This  change,  if  it  also 
involved  the  cardiac  tissues,  would  account  for  many  of  the 
differences  which  exist  between  the  heart  in  early  and  in 
later  hfe.  The  clinical  evidence  in  favour  of  such  a  hardening 
of  the  tissues  of  the  heart  sometimes  taking  place  in  later 
h'fe,  is  so  strong  as  almost  to  amount  to  proof — in  spite  of 
the  fact  that  anatomists  will  tell  us  that  there  are  practically 
no  fibrous  elements  present  in  the  tissues  of  the  heart  wall, 
and  that,  therefore,  a  change  which  involves  the  fibrous  tissues 
of  the  body  generally  caimot  be  expected  to  affect  the  heart 
wall ;  but  if  this  is  really  so,  then  the  change  which  we  often 
detect  clinically  in  the  heart  of  advanced  life  must  be  due 
to  some  corresponding  change  taking  place  in  the  muscular 
fibres  themselves. 

Even  if  this  theory  of  the  heart  wall  itself  partaking  in 
the  increasing  rigidity,  which  age  induces  in  the  fibrous  tissues 
of  the  body,  be  ultimately  proved  to  be  wrong,  and  some  other 
explanation  be  found  for  the  phenomena  here  described,  the 
writer  asks  that  for  the  present  this  theory  be  allowed  to 
stand  provisionally,  if  only  as  a  working  hypothesis,  because 
it  suffices  so  well  to  explain  and  bring  into  line  so  many  of 
the  differences  which  exist  between  the  heart  in  early  and 
in  later  life,  and  helps  to  supply  a  means  of,  to  some  extent, 
bringing  order  into  a  subject  which,  in  the  present  state  of 
our  knowledge,  is  at  best  somewhat  chaotic.  It  is  asked, 
therefore,  that  this  hmitation  be  accepted,  in  connection  with 
the  dogmatic  statements  in  the  following  pages,  by  those  who 
cannot  agree  wholly  with  the  writer  of  them. 

Again,  in  order  to  avoid  misunderstanding,  it  is  desirable 
to  define  clearly  the  sense  in  which  the  word  '  rigidity  '  is 
used  in  this  connection ;  for  the  heart  does  not,  in  the  absolute 
sense  of  the  term,  possess  any  rigidity  at  all.  It  is  used  here 
merely  in  a  relative  sense — for  want  of  a  better  word — and 
when  used  must  be  understood  to  imply  lessened  distensibihty — 
namely,  an  increase  in  the  amount  of  the  opposition  which  the 
cardiac  tissues  (including  the  pericardium)  can  offer  to  any 
force  tending  to  cause  an  alteration  in  the  shape  or  size  of  the 
heart. 


78  DISTENSIBILITY  OF  THE  HEART 

The  word  '  distensible  '  has  been  used  to  describe  the  con- 
dition of  the  heart  in  the  first  two  or  three  decades  of  hfe  ;  for 
it  is  easily  distended,  the  soft  and  still  developing  fibrous 
tissue  of  the  pericardial  sac  having  but  little  controlling  influence 
upon  any  tendency  the  heart  may  have  to  become  enlarged. 
As  the  fibrous  tissues  of  the  pericardium  get  stronger  with  age, 
they  will  exert  more  control  over  the  distensibility  of  the  heart, 
and  to  this  control  is,  in  all  probability,  added  another  agency 
— namely,  a  certain  amount  of  stiffness  or  added  firmness, 
which  the  tissues  of  the  heart  itself  often  seem  to  gain  as  life 
advances. 

This  gradual  change  has  already  been  spoken  of  in  con- 
nection with  the  altered  type  of  dilatation,  which  is  seen  in 
adult  as  compared  with  early  life.  This  same  lessened  tendency 
to  enlargement  (due  to  changes  both  in  the  heart  wall  and  in 
the  pericardium)  goes  on  increasing  with  the  increasing  rigidity 
of  the  tissues  (which  is  apt  to  characterise  advancing  age),  until 
in  later  life  the  heart's  walls  may  so  have  lost  their  distensibility 
that  a  degree  of  overstrain  which  would  have  been  certain  to 
cause  dilatation  earher  in  life  has  now  no  effect  in  enlarging 
the  heart. 

Shortly  to  describe  this  change  in  the  character  of  the 
heart,  it  may  be  called  '  the  gaining  of  an  increasing  degi'ee  of 
rigidity  as  age  advances,'  and  the  less  dilatable  heart  of  later 
life  may  be  called  '  the  relatively  rigid,'  or  simply  '  the  rigid  ' 
heart  of  advanced  life. 

Bat  this  increasing  rigidity  does  not  only  affect  the  ease 
with  which  the  heart  is  dilated.  There  is  every  reason  to  believe 
that  the  heart  walls  are  less  easily  compressed  and  deformed, 
by  the  contractions  of  its  own  muscles,  in  later  life  than  it  is  in 
early  life.  In  other  words  :  that  the  increased  hardening  of  the 
tissues  with  age  involves,  not  only  the  two  layers  of  the  peri- 
cardium, but  also  the  wall  of  the  heart  itself ;  and  that  in  later 
life  the  heart  will,  when  diminished  in  bulk  by  contraction  of 
its  muscles,  tend  to  return  to  its  original  size  with  greater 
force  than  it  does  in  early  life.  Therefore,  after  the  ventricle 
has  been  diminished  in  size  during  the  act  of  contraction,  it 
will,  as  soon  as  the  contractile  force  ceases,  tend  immediately 
to  return  to  its  original  size,  and  in  so  doing,  it  will  suddenly 


IN  LATER  LIFE  79 

increase  the  capacity  of  its  ventricle  and  cause  a  certain 
amount  of  suction  to  be  developed  within  it. 

Now,  here  again,  the  word  *  rigid  '  is  not  very  suitable, 
because  a  rigid  body  is  not  elastic  ;  whereas  the  slight  hardening 
of  the  cardiac  tissues,  which  is  here  spoken  of  as  relative 
rigidity,  does  impart  to  them  some  mechanical  elasticity,  and 
so  gives  the  heart  the  power  of  mechanical  aspiration,  as  well 
as  the  muscular  aspiration  already  described. 

With  these  words  of  explanation  and  apology  as  to  the 
use  of  the  word  '  rigidity,'  and  also  as  to  the  theory  here  pro- 
pounded as  to  the  increasing  resilience  of  the  heart  in  later  life 
being  brought  about  by  the  hardening  and  consohdation  of 
its  tissues,  we  will  proceed  to  deal  with  the  bearings  of  this 
theory  upon  the  symptoms  and  signs  of  the  more  extreme 
cases  of  cardiac  weakness  in  later  hfe. 

Eesults  of  increased  rigidity  of  its  tissues  so  far  as  the  heart 
ITSELF  is  concerned. — In  the  first  place  the  increase  in  firmness, 
which  we  are  assuming  that  age  is  hkely  to  impart  to  the 
cardiac  tissues,  will — as  already  pointed  out — lessen  both  the 
readiness  with  which  the  wall  of  the  heart  dilates  when  exposed 
to  abnormally  gi-eat  intraventricular  pressures,  and  also  make 
it  resist  other  types  of  deformation  as  well.  We  shall  not, 
therefore,  expect  to  find  in  later  hfe  the  gi*eat  diminution  in 
the  size  of  the  heart  of  which  we  have  already  spoken  when 
dealing  with  extreme  cardiac  weakness  in  early  life. 

But  this  increased  resistance  to  change  of  form  will  affect 
the  diminution  in  the  size  of  the  full  heart  in  another  way — 
namely,  by  interfering  to  some  extent  with  the  compensatory 
mechanism  whereby  the  lessening  in  size  of  the  heart  is  brought 
about.  When  the  distensible  heart  of  an  adolescent  has  con- 
tracted, its  soft  fibrous  elements,  having  but  little  resihency, 
can  take  but  little  part  in  restoring  the  ventricle  to  its  original 
shape,  and  this  has  to  be  done  by  muscular  expansion  alone. 
In  later  life,  however,  the  tissues  of  the  heart  being  more 
rigid,  there  will  be  more  inherent  tendency — apart  from  mus- 
cular expansion — for  the  ventricle  to  return  to  its  full  size 
as  soon  as  contraction  is  over.  In  other  words  :  this  quality 
of  the  tissues  will  ensure  the  heart  having  a  certain  amount 


80  DISTENSIBILITY  OF  THE  HEART 

of  mechanical  elastic  recoil  in  addition  to  its  power  of  muscular 
expansion. 

When  dealing  with  the  mechanism  which  ensured  the 
underfilling  of  the  heart  in  extreme  muscular  weakness,  we 
pointed  out  that  expansion  being  a  less  effective  action  than 
contraction,  it  might  reasonably  be  expected  that  it  would 
diminish  in  effectiveness  to  at  least  as  great  an  extent  as 
was  the  case  with  contraction,  and  that  therefore  in  a  heart 
which  filled  itself  solely  by  its  own  muscular  expansion  muscular 
weakness  might  be  expected  to  interfere  with  the  filling  quite 
as  much  as  with  the  evifdying  of  the  ventricle,  and  that  in 
all  probability  defective  filling  would  be  the  first  of  the  two 
phenomena  to  develop. 

Now,  in  later  life  the  possession  of  the  mechanical  resilience 
of  which  we  are  speaking  must,  to  some  extent,  interfere  with 
this  compensatory  mechanism  by  giving  the  heart  the  power 
of  mechanical  aspiration  in  addition  to  that  due  to  muscular 
expansion.  We  can,  therefore,  say  that  there  is  good  reason 
to  expect  that  in  later  life  there  will  be  more  complete  filling 
of  a  muscularly  weak  ventricle  than  would  be  the  case  in 
early  life. 

In  other  words  :  in  later  Ufe,  we  must  not  expect  to  find 
clinically  such  marked  diminution  of  the  cardiac  dullness  in 
cases  of  myocardial  weakness  as  is  the  case  in  early  life. 

The  firmness  of  the  fibrous  tissues  in  maturity  may  help 
to  bring  about  this  same  result  in  another  way,  for  some  of  the 
apparent  diminution  in  the  size  of  the  cardiac  area,  when  the 
patient  lies  on  his  back,  may  be  due  to  the  underfilled  heart 
falling  away  from  the  chest  wall  to  a  greater  extent  than 
normal.  This  also  would  be,  in  some  measure,  less  in  extent 
when  the  tissues  of  the  heart  and  the  mediastinum  were  firm 
than  when  they  were  soft. 

We  find,  therefore,  that  while  smallness  of  the  full  heart 
(from  underfilhng)  is  an  almost  certain  accompaniment  of 
extreme  muscular  weakness  in  adolescence  and  early  life,  in 
middle  and  later  life,  on  the  other  hand,  this  diminution  in 
size  cannot  be  expected  to  occur  to  the  same  extent,  and  may 
even  be  absent  altogether,  so  far  as  our  powers  of  observation 
are  concerned. 


IN    LATER  LIFE  81 

It  may,  therefore,  I  think,  be  stated^that  just  as  the  degree 
of  distensibihty  of  a  heart  that  is  only  moderately  weak  is 
shown  by  the  type  and  the  extent  of  its  enlargement,  so,  on  the 
other  hand,  the  degree  of  distensibihty  of  an  extremely  weak 
heart  is  shown  by  the  extent  of  its  dvminutimi  in  size.  The 
more  distensible  the  heart  the  gi-eater  will  be  the  diminution 
in  size  of  the  heart  when  full,  and  the  less  the  distensibihty, 
the  less  \vill  be  that  diminution. 

Although  the  possession  of  mechanical  elastic  recoil  is 
here  only  inferred  from  the  clinical  phenomena  which  the  heart 
exhibits,  it  is  possible  that  the  difference  between  the  heart 
of  early  and  later  hfe  in  this  respect  may  be  demonstrable  by 
experiment  in  the  post-mortem  room,  and  it  would  certainly 
be  an  interesting  field  for  research.  It  is  not,  however,  at  all 
certain  that  it  would  be  demonstrable,  because  of  the  presence 
of  rigor  mortis — for  the  rigidity  of  the  muscles  would  far  exceed 
any  elasticity  which  the  scanty  fibrous  elements  of  the  heart 
might  be  expected  to  be  capable  of.  Moreover,  it  is  possible 
that  the  formed  elements  of  the  muscular  fibres  themselves 
may  play  an  important  part  in  producing  the  phenomenon 
which  we  are  now  discussing.  If  this  be  so,  it  is  not  easy 
to  see  how  after  death  this  quahty  could  be  demonstrable. 

The  possession  of  some  measm-e  of  mechanical  elastic 
recoil  may,  therefore,  be  taken  as  an  important  characteristic 
differentiating  the  heart  of  middle  and  later  hfe  from  that  of 
early  hfe,  and  one  upon  which  some  of  the  many  clinical 
differences  between  hearts  at  those  two  periods  of  life 
depend. 

More  stress  must  not  be  laid  upon  this  point  than  it  will 
rightly  bear,  for  it  must  be  remembered  that  anatomically 
there  appears  httle  or  no  fibrous  tissue  in  the  heart  waU,  and 
also  if  mechanical  resihence  be  granted,  the  force  which  brings 
it  into  play  is,  after  aU,  the  contractile  power  of  the  heart 
wall,  and  that  when  a  heart  is  weak  its  more  feeble  systohc 
squeeze  wiU  be  followed  by  only  a  feeble  elastic  rebound. 
Therefore,  unless  the  heart  be  very  rigid,  there  will  be  some 
compensatory  diminution  in  its  fullness,  and  the  difference 
between  the  smallness  of  the  heart  in  the  distensible  and  the 
relatively  rigid  heart  will  only  be  one  of  degree. 


82  DISTENSIBILITY  OF  THE  HEART 

In  the  case,  on  the  other  hand,  of  a  heart  which  combines 
considerable  weakness  with  a  considerable  degree  of  rigidity, 
it  is  probable  that  the  weak  muscle  will  be  miable  fully  to 
compress  the  relatively  inelastic  heart  walls,  and  that  there 
will  be  incomplete  emptying  of  the  heart  at  each  systole. 

If  this  be  so,  the  effect  upon  the  general  circulation  will 
be  the  same  as  when  an  underfilled  ventricle  completely  empties 
itself ;  for  in  both  cases  a  portion  only  of  the  normal  amount 
will  be  discharged  into  the  arteries  at  each  contraction,  and, 
in  this  type  of  heart,  the  weaker  the  heart  muscle  the  less  perfect 
will  be  the  emptying  of  the  ventricle  during  its  contraction. 

Therefore,  in  this  case  also,  we  can  estimate  clinically,  by 
the  extent  of  the  deficiency  in  the  amount  of  blood  in  active 
circulation,  the  extent  of  the  muscular  weakness  of  the  heart. 

It  has  been  already  pointed  out  that  in  adolescence,  owing 
to  its  power  of  aspiration  failing  before  its  power  of  expulsion, 
the  risk  of  sudden  death  from  asystole  is  reduced  to  a  minimum  ; 
whereas  in  later  life  the  possession  of  mechanical  resilience 
deprives  the  heart  of  this  safeguard,  and  therefore  sudden 
death,  due  to  the  left  ventricle  receiving  a  larger  amount  of 
blood  than  it  has  power  to  expel,  is  by  no  means  an  uncommon 
accident  in  cases  of  extreme  myocardial  weakness. 

Further,  in  cases  where  death  does  not  follow  in  such  a  case, 
anginous  pain  is  caused  by  the  efforts  of  the  ventricle  to  exert 
a  force  beyond  what  it  is  readily  capable  of  doing.  This  is, 
I  believe,  one  explanation  of  the  fact  that  anginous  pain  in 
simple  myocardial  weakness  is  rare  in  early  life,  but  by  no 
means  uncommon  in  later  life. 

In  valvular  disease  where,  in  consequence  of  valvular 
incompetence  and  the  resulting  regurgitation,  over-filling  of 
the  leit  ventricle  can  occur,  angmous  pain  is  frequent  in  early, 
just  as  in  later,  life. 

Before  leaving  this  subject  of  distensibility  of  the  heart  in 
later  life,  it  is  necessary  to  draw  attention  to  the  fact,  already 
pointed  out,  that  there  is  great  variation  in  the  amount  of 
distensibility  possessed  by  the  heart  in  later  life,  just  as  was 
shown  to  be  the  case  in  early  adult  life. 

For,  while  in  some  patients  the  heart  appears  to  be  so  rigid 


IN  LATER  LIFE  83 

that  it  hardly  seems  to  dilate  at  all  under  circumstances  that 
would  certainly  have  caused  marked  dilatation  earlier  in  life, 
we  may,  on  the  other  hand,  sometimes  meet  with  patients  in 
whom  at  the  age  of  sixty  the  heart  appears  to  dilate  nearly  as 
readily  and  in  the  same  manner  as  it  would  do  in  a  patient  only 
thirty  years  of  age. 

It  need  not  be  pointed  out  that,  so  far  as  the  general  fibrous 
tissues  of  the  body  are  concerned,  we  expect  such  variations  ; 
for  one  man  will  remain  hssom  and  active  till  he  is  over  sixty, 
whereas  another  will  become  stiff  and  aged  before  that  time. 

It  may  be  of  interest  to  give  some  details  of  two  elderly 
ladies,  in  whom  the  heart  was  distensible  and  '  young,'  for 
comparison  with  two  other  cases,  which  are  given  at  pp.  87 
and  89,  in  whom  the  heart  was  rigid  and  old. 

The  patient  was  a  lady  aged  sixty-two,  who  was  suffering 
from  tachycardia,  which  ultimately  showed  signs  of  becoming  a 
true  exophthalmic  goitre,  and  was  cured  by  a  partial  excision 
of  the  thyroid. 

When  seen  by  the  writer,  her  heart  was  much  dilated  and 
was  beating  140  to  the  minute.  This  was  in  part  due  to  the 
presence  of  the  consulting  physician,  but  its  rate  never  fell 
below  100. 

Her  urgent  cardiac  symptoms  dated  some  months  back, 
and  w^ere  brought  on  after  an  '  influenzal '  attack  by  a  series 
of  somewhat  trivial  causes — showing  that  the  heart  was  in  a 
very  over-sensitive  condition. 

Firstly,  slight  over-exertion  brought  on  an  attack  of  asthma 
followed  by  cardiac  dilatation  and  a  mitral  murmur.  On  re- 
covery, too  long  a  drive  caused  a  return  of  the  symptoms  and 
a  pulse  rate  of  140  with  occasional  extra  systoles. 

The  cardiac  action  was  very  excited,  and  the  sounds  so 
loud  that  they  were  audible  when  the  stethoscope  was  one- 
ttiird  of  an  inch  away  from  the  chest  wall. 

The  apex  beat  was  in  the  fifth  interspace,  about  midway 
between  the  left  nipple  line  and  the  anterior  axillary  line, 
and  there  was  enlargement  of  the  cardiac  area  upwards  and 
to  the  left.  There  was  no  dilatation  to  the  right  or  down- 
wards, and  the  right  lung  crossed  over  the  middle  line  and 
was  well  to  the  left  of  the  sternum  in  the  fourth  and  fifth 
interspaces,  and  during  full  expiration  the  edge  of  the  right 

g2 


84 


DISTENSIBILITY  OF  THE  HEART 


Adolescent'  Type  of  Dilatation 
occiTERiNG  IK  Late  Adtlt  Life 


lung  only  retreated  as  far  as  the  left  border  of  the  sternum  in 
the  fourth  left  interspace — thus  showing  either  displacement 
of  the  heart  towards  the  left  or  diminution  in  the  size  of  the 
right  ventricle. 

The  dilatation  was  wholly  outwards  and  to  the  left,  and 
the  relative  dullness  extended  well  beyond  the  left  nipple  line 
in  both  the  third  and  fourth  interspaces. 

The  only  murmur  was  a  faint  mitral  one,  and  there  was 

an  extra  sound  audible 
over  the  right  ventricle 
which  was  probably  a  third 
sound ;  but  as  the  heart 
was  beating  140  to  the 
minute,  the  proper  place 
for  the  third  sound  would 
be  less  than  one-tenth  of  a 
second  before  the  succeed- 
ing contraction,  and  there- 
fore it  would,  as  was  the 
case  here,  appear  Uke  a 
redupHcation  of  the  first 
sound,  although  with  such 
a  limited  area  of  audition 
as  to  preclude  the  possi- 
bility of  this  explanation. 
Fig.  6. 

The     striking     feature 
about    this   case  was    the 
fact  that  the  mode  of  dila- 
tation of  the  heart  was  that  of  an  adolescent  and  not  of  a 
woman  of  sixty-two. 

There  was  in  this  case  no  evidence  of  any  dilatation  of  the 
left  ventricle  other  than  the  outward  displacement  of  the  apex ; 
for  the  cardiac  sounds  were  heard  less  loudly  than  normal 
over  the  situation  of  the  left  ventricle  and  the  left  auricle, 
posteriorly. 

The  pecuhar  shape  of  the  dilated  heart  was  probably  due, 
as  is  the  case  in  anaemic  dilatation,  to  two  factors  :  firstly,  the 
distensibility  of  the  anterior  wall  of  the  right  ventricle  ;  and 
secondly,  to    the  occurrence    of    a    dilatation    of    the    right 


Mrs.  S.,  aged  fifty-two.  Shows  upward 
dilatation  of  the  right  ventride,  the  result  o£ 
overstrain. 


IN  LATER  LIFE  &5 

ventricle,  combined  with  a  left   ventricle  of  normal  or  less 
than  normal  size. 

The  second  case  is  that  of — 

A  lady  aged  fifty-two,  who  came  to  see  me  for  heart  weakness, 
which  showed  itself  not  only  by  some  breathlessness  on  exer- 
tion but  also  a  great  sense  of  feebleness  and  want  of  energy. 
There  was  no  evidence  of  a3dema  of  the  ankles  or  cyanosis. 

The  heart  was  fomid  to  be  markedly  dilated  upwards  and 
to  the  left,  just  as  occurs  in  overstrain  in  adolescence. 

There  was  some  relative  dullness  and  pulsation  in  the  second 
left  interspace  and  well-marked  pulsation  in  the  third  interspace 
with  relative  dullness  extending  some  3^  inches  from  the 
sternum.  The  absolute  dullness  just  reached  into  the  third 
interspace.  The  apex  was  high  in  the  fifth  interspace  well 
external  to  the  nipple  line.  The  liver  dullness  was  small. 
There  was  no  murmur  at  the  apex   (see  fig.  6). 

If  the  diagram  here  given  is  compared  with  figs.  48,  99, 
the  similarity  of  the  dilatation  here  to  that  occurring  in  ado- 
lescence will  be  evident.  The  patient  did  not,  however,  recover 
with  the  rapidity  of  an  adolescent,  and  needed  prolonged  rest 
and  care. 

Such  cases  are,  however,  rare,  and  as  a  rule  the  manner 
and  the  amount  of  the  dilatation  seem  to  point  to  the  fact 
that  the  rigidity  of  the  heart  wall  increases  steadily  as  age 
advances. 


Early  Diagnosis  of  Heart  Failure  with  Enlargement 
IN  Relatively  Eigid  Hearts 

In  the  relatively  rigid  heart  of  advanced  hfe,  when 
dilatation  occurs,  we  find  it  to  be  of  the  same  type  as  that 
already  described  at  p.  31,  as  occurring  in  adult  hfe.  The 
principles, therefore,  governing  its  early  diagnosis  are  the  same 
as  those  there  given.  It  must,  however,  be  remembered  that 
owing  to  the  possibility  in  later  life  of  the  cardiac  tissues 
being  less  distensible  it  must  not  be  concluded  that  a  slight 
degree  of  enlargement  at  this  time  of  life  means  only  the  shght 
amount  of  overstrain  that  it  would  mean  in  early  adult  hfe. 


86  HEART  FAILURE 

Considering  the  degree  in  which  rigidity  of  the  pericardium 
and  of  the  walls  of  the  heart  can  limit  the  heart's  distensibility 
an  endeavour  must  be  made  to  estimate  what  the  degree  of 
distensiblity  is,  before  any  estimate  can  be  made  of  the 
amount  of  overstrain  which  any  particular  amount  of  dilatation 
represents. 

Some  help  in  this  estimation  may  be  sometimes  gained 
by  noticing  the  general  build  and  habit  of  the  patient,  but  the 
only  reliable  guide  in  judging  of  the  amount  of  overstrain 
is  obtained  from  noting  the  strength  of  the  right  ventricular 
beat  as  shown  by  the  heart  sounds  and  the  condition  of  the 
veins,  and  especially  by  study  of  the  pulse  in  the  jugular  bulb. 
If  we  find  distinct  evidences  of  considerable  overaction  of  the 
right  ventricle,  combined  with  but  slight  enlargement  of  the 
heart,  we  must  lay  stress  upon  the  overaction  which  we  can 
notice,  and  conclude  that  the  absence  of  a  more  noticeable 
amount  of  dilatation  must  be  due  to  rigidity  of  the  heart 
walls.  But  if  we  find  a  moderately  acting  right  heart  combined 
with  slight  enlargement,  we  are  at  once  at  a  loss,  so  far  as  the 
estimation  of  the  amount  of  its  failure  is  concerned  ;  for  the 
case  may  be  one  of  rigid  heart  with  a  muscularly  weak  right 
ventricle,  and  in  a  condition  of  severe  overstrain,  in  spite  of 
the  slightness  of  the  venous  phenomena. 

This  is  but  an  instance  of  the  caution  necessary  in  later 
life  as  regards  reliance  upon  negative  phenomena. 

A  phenomenon  that  is  certainly  abnormal  is  of  value, 
but  an  apparently  normal  one  has  not  the  same  value. 

In  later  life,  as  under  many  other  circumstances,  a  reliable 
diagnosis  cannot  be  made  till  all  the  facts  of  the  case  have 
been  considered  and  their  due  value  apportioned  to  them  in 
the  light  of  all  the  phenomena  observed. 

Heart    Failure    without    Enlargement    in    Strong    or 
ONLY    Moderately    Weak   Hearts    of    Considerable 

ElGIDITY 

As  has  already  been  pointed  out,  the  development  of  the 
marked  '  rigidity  '  which  we  occasionally  find  in  the  heart 
of  later  life  necessitates  the  formation  of  a  fresh  group  in 


WITHOUT  ENLARGEMENT  87 

addition  to  the  two  gi-oups  of  '  strong  heart  with  enlarge- 
ment,' and  '  weak  heart  without  enlargement,'  which  included 
practically  all  cases  of  cardiac  failure  in  early  life. 

In  this  gi'oup,  we  shall  deal  with  cases  where  the  pericardium 
and  heart  wall  have  so  lost  their  distensibility  (as  a  result  of 
senile  or  other  changes)  that  a  rise  of  intraventricular  pressure 
which,  earher  in  life,  would  have  been  certain  to  cause  dilatation 
of  the  heart,  is  now  powerless  to  do  so — so  far  at  least  as  our 
powers  of  clinical  observation  are  concerned. 

The  difficulties  in  the  way  of  a  correct  diagnosis  of  heart 
failure  are  in  later  Hfe  greatly  added  to  by  the  recognition  of 
the  fact  that  we  must  not  (owing  to  the  rigidity  of  the  heart) 
expect  dilatation  under  circumstances  that  would  certainly 
cause  it  earlier  in  life. 

This  also  must  limit  the  number  of  simple  cases  with  cardiac 
dilatation  which  we  are  likely  to  meet  with,  while  it  adds  to  the 
number  of  the  more  complex  and  difficult  cases  where  heart 
failure  is  unaccompanied  by  enlargement. 

No  hard-and-fast  line  can  be  drawn  between  these  cases 
and  those  in  the  last  group ;  for  the  strength  of  which  we  are 
assuming  the  heart  is  possessed  is  adequate  to  dilate  a  normal 
heart  wall  though  not  an  unduly  rigid  one,  and  under  some 
circumstances  there  may  quite  possibly  be  some  dilatation  of 
ventricles  or  auricles  although  there  be  no  clinical  evidence  of 
it.  Practically,  this  group  belongs  to  the  preceding  one  of 
heart  failm-e  with  enlargement,  but  for  purposes  of  clinical 
diagnosis  it  is  convenient  to  separate  it. 

If  we  regard  the  '  auriculo-venous  reservoir  '  {vide  p.  132) 
as  part  of  the  heart  proper,  we  should  have,  even  in  these  cases, 
to  speak  of  cardiac  dilatation  being  present. 

The  first  of  the  following  cases  is  one  of  these  border-line 
ones,  and  will  serve  to  illustrate  this  gi'oup,  though  it  was  not 
possible  absolutely  to  exclude  the  presence  of  some  cardiac 
dilatation.  In  the  second  case  here  recorded,  there  was  certainly 
no  cardiac  enlargement. 

The  diagnosis  of  this  group  of  cases  is  well  illustrated  by 
the  accounts  here  given. 

The  first  case  is  that  of  an  elderly  man  with  well-marked 
arcus  senilis  and  atheromatous  radial  and  temporal  arteries, 


88  HEAET  FAILURE 

who  was  admitted  to  hospital  suffering  from  breathlessness 
and  a  certain  amount  of  dropsy  of  the  ankles.  The  heart  was 
very  slightly,  if  at  all,  enlarged. 

There  was,  however,  well-marked  venous  pulsation  in  the 
neck,  showing  that,  although  the  muscular  strength  of  the 
ventricles  was  not  great  enough  to  cause  material  dilatation 
of  their  cavities,  that  of  the  right  was  sufficient  to  keep  the 
veins  fully  distended  and  pulsating. 

There  was,  moreover,  a  loud  systolic  murmur  heard  in  the 
second  and  third  right  interspaces,  and  well  conducted  up  into 
the  vessels  of  the  neck.  This  murmur,  by  its  character — its 
area  of  audition  and  its  direction  of  conduction — very  closely 
resembled  an  aortic  systolic  murmur.  This  case  is  impressed 
upon  the  writer's  memory  by  the  fact  that  his  house-physician, 
who  was  a  keen  observer  and  a  young  man,  fearlessly  opened 
the  following  discussion  in  answer  to  his  chief's  suggestion 
that  this  murmur  was  produced  in  the  superior  cava  and  was 
a  sign  of  tricuspid  regurgitation.  He  said  :  '  Why  make  such 
a  foolishly  fanciful  diagnosis  ?  Here  we  have  an  oldish  man 
with  well-marked  arcus  senihs  and  atheromatous  arteries,  and 
just  the  patient  in  whom  one  would  suspect  atheromatous 
roughening  of  the  aorta  and  an  aortic  systolic  murmur.'  To 
this  the  answer  was  :  '  I  am  sorry,  but  my  fingers  tell  me  that 
these  are  dilated  veins  in  which  the  murmur  is  heard,  and  my 
ears  tell  me  that  this  murmur  is  very  loud  over  the  second 
interspace  and  not  nearly  so  loud  in  the  arteries  of  the  neck 
as  an  arterial  murmur  would  be.  If  the  blood  in  the  aorta 
were  vibrating  enough  to  make  a  loud  murmur  audible  through 
the  inch  of  lung  tissue  between  it  and  the  chest  wall,  that  same 
blood,  a  fraction  of  a  second  later,  when  it  reaches  the  carotid 
arteries,  must  be  still  vibrating ;  and  with  a  stethoscope  appHed 
directly  on  to  the  artery  the  murmur  would  be  better  heard 
than  this  one  is.  Moreover,'  I  added,  '  this  murmur  is  well 
heard  low  down,  in  the  second,  and  also  in  the  third,  interspace 
in  a  manner  that  an  aortic  systolic  murmur  is  not.' 

These  facts  did  not  satisfy  the  young  observer,  and,  although 
a  few  days'  rest  in  bed — a  little  strophanthus  and  salicine — 
sufficed  entirely  to  remove  the  dropsy,  the  over-distension  of 
the  veins,  and  the  murmur,  when  the  notes  of  the  case  were 
put  away  ready  for  binding,  I  noticed  that  the  diagnosis  was 
entered  up  as  '  aortic  systohc  murmur.' 

Such  a  case  as  this  shows  that  in  a  relatively  rigid  heart 


WITHOUT  ENLARGEMENT  89 

I  we  cannot  depend — for  the  early  diagnosis  of  heart  failure — 
upon  changes  in  either  the  right  or  left  ventricle  as  signs  of 

1  dilatation,  or  upon  the  presence  of  systolic  murmurs — although 
the  latter,  when  present,  are  of  great  value — but  we  may  have 
to  depend  entirely  upon  phenomena  due  to  over-distension 
of  the  great  veins.     This  case  is  also  referred  to  at  p.  222. 

The  following  is  another  border-hne  case  in  which  a  degree 
of  muscular  weakness  as  well  as  rigidity  of  the  heart  wall 
brings  it  nearer  still  to  the  cases  of  heart  failure  without 
enlargement,    which   will  be   next   dealt  with. 

The  patient  was  a  stout,  red-faced  man,  aged  forty-four, 
whose  work  as  an  agent  involved  a  good  deal  of  cycling.  For 
many  months  he  had  noticed  an  increasing  breathlessness,  and 
he  had  been  unable  to  do  much  cychng  for  more  than  a  year. 
Within  the  last  few  weeks,  his  breathlessness  had  been  so 
troublesome  that  he  came  to  the  hospital  and  was  admitted. 
There  had  been  no  swelling  of  the  ankles  and  no  fainting  attacks. 
On  admission,  the  most  evident  signs  of  cardiac  failure  were 
fullness  of  the  veins  of  the  neck  with  well-marked  pulsation  in 
them  as  far  up  as  the  angle  of  the  jaw ;  but  the  pulsation,  though 
greater  in  extent,  was  less  forcible  than  in  the  last  case.  The 
pulse  was  small  in  volume  and  wanting  in  vigour,  the  tension 
was  rather  high  and  the  blood  pressure,  as  tested  by  the  sphyg- 
momanometer, was  160  mm.  of  mercury. 

As  regards  the  heart.  Instead  of  finding  distinct  dilatation, 
and  perhaps  a  tricuspid  murmur,  as  might  be  expected  under 
such  circumstances,  percussion  showed  the  cardiac  area  to  be 
normal,  and  on  palpation  and  inspection  the  cardiac  action  and 
impulse  were  found  to  be  more  feeble  than  normal. 

Auscultation  confirmed  this  ;  for  the  heart  sounds  were 
decidedly  weak,  and  those  at  the  apex  were  short  and  sharp, 
suggesting  feebleness,  and  there  was  also  a  very  faint  systolic 
murmur  present.  The  right  ventricular  sounds,  while  rather 
better  than  those  at  the  apex,  were  not  as  loud  as  normal,  and 
there  was  no  murmur.  As  regards  the  lungs,  there  was  no 
emphysema,  but  there  was  a  good  deal  of  bronchial  wheeze, 
suggestive  of  bronchial  catarrh  with  some  bronchial  spasm. 

Here,  again,  we  were  dealing  with  a  case  of  heart  failure 
without  manifest  dilatation,  although  some  dilatation  of 
the  right  auricle  and  possibly    of  the  right  ventricle  might 


90  HEART  FAILURE 

nevertheless  exist,  and  the  mitral  systolic  murmur  suggested 
left  ventricular  dilatation.  The  explanation  of  such  a  case  is 
probably  as  follows  :  The  man  had  been'  suffering  more  or 
less  for  some  time  from  a  gi'adually  rising  blood  pressure — the 
result  probably  of  failing  kidney  action  or  an  injudicious  dietary, 
and  the  nutrition  of  the  heart  had  not  been  sufficient  (owing  to 
faulty  coronary  arteries)  to  enable  it  to  keep  pace  with  the 
extra  work  thus  thrown  upon  it.  Had  it  done  so,  there  would 
have  been  a  measure  of  hypertrophy  with  heart  sounds  louder 
than  normal  and  a  murmur  due  to  tricuspid  regurgitation. 
The  final  cause  of  his  breakdown  was  doubtless  his  bronchial 
trouble.  The  fact  of  having  a  heart  of  normal  size  and  weak 
action,  in  face  of  a  blood  pressure  of  160  mm.  of  mercury, 
suggests  myocardial  degeneration  from  malnutrition  (see 
p.  144). 

The  distension  and  pulsation  of  the  veins  showed  that  the 
right  ventricle  was  relatively  strong  and  was  endeavouring  to 
compensate  for  the  defective  action  of  the  left  heart. 

As  regards  the  treatment  :  the  bronchial  catarrh  and 
spasm,  though  only  slight,  had  to  be  dealt  with,  and  also  small 
doses  given  of  such  a  drug  as  strophanthus  which,  while  not 
increasing  arterial  contraction,  does  increase  the  vigour  of  the 
cardiac  action,  and  so  tends  to  improve  the  cardiac  nutrition. 
Digitalis  would  not  be  indicated.  A  very  important  part  of 
the  treatment  of  such  a  case  is  the  lessening  of  the  peripheral 
resistance  by  means  of  drugs  such  as  the  saHcylates.  In  this 
case,  however,  the  prognosis  was  not  hopeful  as  in  the  last  one, 
owing  to  the  myocardial  weakness.  This  was  shown  by  his 
rate  of  progress  ;  for,  although  the  heart  sounds  gained  in  vigour 
after  three  weeks'  rest  in  bed,  combined  with  the  treatment 
described,  the  man  progressed  but  slowly. 

These  two  cases  will  suffice  to  show  the  points  upon  which 
the  early  diagnosis  of  heart  failure  in  relatively  rigid  hearts 
must  depend. 

Breathlessness,  combined  with  fullness  and  pulsation  of  the 
veins  are  the  first  signs.  In  a  moderately  strong  heart  there 
wiU  be  a  systolic  murmur  due  to  tricuspid  regurgitation :  either 
a  true  tricuspid  systolic  with  or  without  a  superior  vena  cava 
murmur,    or    else   the  latter   murmur  alone,  and  there   will 


WITHOUT  ENLAEGEMENT  91 

probably  be  a  mitral  systolic  murmur  as  well.  In  a  weaker 
heart  the  right  ventricle,  while  strong  enough  to  cause  some 
regurgitation  into  the  neck  veins,  may  yet  be  unable  to  develop 
enough  pressure  to  give  rise  to  a  murmur  at  the  tricuspid 
orifice  or  in  the  superior  vena  cava. 

If  the  heart  were  weaker  still,  it  would  come  into  the  group 
(now  to  be  discussed)  of  '  Heart  Failure  without  Enlargement 
in  Weak  Hearts.' 

Heart  Failure  without  Enlargement  in  Decidedly 
Weak  and  Eelatively  Eigid  Hearts 

The  most  difficult  of  all  the  groups  into  which  we 
have  divided  cases  of  heart  failure  in  later  life  has  now  to  be 
discussed — ^namely,  the  group  which  contains  cases  where  the 
myocardium  is  too  weak  to  cause  any  dilatation  of  even  a 
normally  distensible  heart  wall. 

After  what  has  already  been  said  as  to  the  variations  in 
the  distensibility  of  the  heart,  it  must  not  bo  forgotten  that 
even  in  later  life  an  exceptional  case  may  be  met  with  to  which 
the  description  already  given  (p.  56)  of  the  muscularly 
weak  heart  of  adolescence  would  apply.  But  in  the  majority 
of  the  cases  of  this  type  met  with  in  later  hfe  the  signs  and 
symptoms  are  modified  by  the  increase  in  the  firmness  and 
resiliency  of  the  heart  wall  which  has  already  been  fully 
discussed. 

In  this  place,  we  shall  simply  take  up  the  main  diagnostic 
points  upon  which  we  must  rely  for  the  recognition  of  heart 
failure  in  such  cases,  together  with  one  or  two  illustrative 
cases,  and  postpone  to  p.  112  the  discussion  of  the  many  and 
serious  complexities  and  uncertainties  which  we  are  only  too 
apt  to  meet  when  studying  the  signs  and  symptoms  of  heait 
failure  in  later  life. 

First,  as  to  symptoms  of  heart  failure.  As  has  already 
been  pointed  out,  the  negative  character  of  much  of  the  evidence 
in  this  class  of  case  renders  it  more  necessary  than  in  early 
life  to  rely  upon  symptoms  of  cardiac  failure.  Owing  to  the 
uncertainty  which  often  attaches  to  the  symptoms  of  any 
ailment,  we  must  be  specially  careful  in  our  analysis  of  them 


92  HEART  FAILURE 

and  not  take  too  much  for  granted  when  we  hear  of  a  patient 
having  breathlessness,  pain,  or  faintness. 

This  question  of  the  proper  analysis  of  symptoms  of  heart 
faihire  will  be  dealt  with  subsequently.  They  will  here  simply 
be  enumerated. 

Dyspnoea. — In  the  first  place,  wo  must  rely  very  largely 
upon  breathlessness  in  our  recognition  of  cardiac  failure  in 
later  life,  and  we  must  be  careful  to  put  due  weight  upon  this 
symptom  and  not  to  pass  it  by  as  not  very  important,  because 
it  is  unaccompanied  by  any  clearly  marked  signs  of  cardiac 
failure  (vide  p.  124).  It  may  positively  be  the  only  well- 
marked  symptom  of  an  amount  of  fatty  degeneration  of  the 
heart  muscle  that  is  seriously  endangering  the  patient's  life. 

In  any  case  where  any  dyspnoea  exists  in  later  life  it  is 
advisable  personally  to  test  the  patient's  power  of  walking 
upstairs  or  of  fast  walking  across  a  room,  and  to  note  the 
amount  of  cardiac  disturbance  that  results  and  the  time  that  it 
takes  for  the  heart  to  recover  from  the  effects  of  the  exercise. 

It  is  hardly  necessary  in  this  connection  to  draw  attention 
to  the  importance  of  making  as  sure  as  possible  that  the 
dyspnoea  is  of  cardiac  and  not  pulmonary  origin  ;  and  if  of 
cardiac  origin  that  it  is  not  due  simply  to  reflex  cardiac 
disturbance  and  therefore  does  not  imply  organic  disease  of 
the  heart.  (For  the  further  discussion  of  this  symptom,  see 
p.  113.) 

Faintness. — In  cases  where  the  left  ventricle  is  mainly 
affected,  faintness,  with  or  without  actual  fainting,  is  a  very 
important  sign  of  muscular  weakness  ;  but  here,  again,  there  is 
great  liability  of  mistaking  fainting  attacks  due  to  Meniere's 
disease  for  those  of  cardiac  origin,  or,  on  the  other  hand,  of 
mistaking  slight  attacks  of  faintness  or  vertigo,  really  due  to 
failing  heart,  for  reflex  attacks  of  gastric  origin.  Such  cases 
are   described  at  p.  121. 

Weariness  and  Leg  Pains. — Associated  with  faintness 
there  may  be  undue  weariness  on  exertion  and  sometimes 
definite  pains  in  the  calves  of  the  legs,  which  become  so  severe 
that  the  patient  has  to  stop  and  rest  for  a  minute  or  two  before 
he  can  recommence  exertion. 

This  is  reall}^  one  of  the  types  of  '  intermittent  lameness,' 


WITHOUT  ENLARGEMENT  93 

and  is  due  to  the  heart  muscle  being  unable  to  keep  up  sufficient 
circulation  in  the  muscles  to  supply  their  needs.  Consequently, 
after  walldng  a  certain  distance,  fatigue  is  established  and  the 
exercise  cannot  be  recommenced  till  the  nutrition  of  the 
muscles  has  recovered  itself. 

For  this  reason,  a  man  with  myocardial  wealmess  may  be 
compelled  to  rest  every  two  hundred  or  three  hundred  yards. 

Such  a  patient,  when  asked  as  to  his  powers  of  walking, 
will  tell  you  that  when  walking  uphill  he  is  stopped  by  breath- 
lessness  and  has  to  rest,  whereas  on  the  level  he  has  to  rest 
'  because  of  tiredness,'  and  it  is  only  on  questioning  him  that 
he  thinks  it  worth  while  telling  you  that  the  tiredness  is 
really  an  uncomfortable  aching  in  the  calves  of  the  legs. 
This  subject  is  fully  dealt  with  in  the  Essay  on  Leg  Pains  of 
Cu'culatory  Origin. 

In  connection  with  these  two  symptoms  of  dyspnoea  and 
faintness,  it  must  be  remembered  that  they  give  some  indication 
by  their  relative  amount  as  to  whether  the  right  or  the  left 
ventricle  is  the  weakest. 

A  man  vvdth  a  strong  left  ventricle  and  a  weak  right  one 
will  be  able  to  walk  about  and  work  till  stopped  by 
breathlessness,  as  in  the  case  of  the  man  referred  to  at  p.  156  ; 
whereas,  when  the  right  ventricle  is  strong  and  the  left  weak 
the  patient  will  only  get  breathlessness  on  very  considerable 
exertion,  and  then  of  an  alarming  type,  his  ordinary  activity 
being  cm-tailed  by  weariness,  faintness,  or  giddiness.  This 
latter  patient  is  far  more  apt  to  have  the  serious  condition 
of  his  heart  overlooked  than  is  the  former,  and  he  is  also  more 
likely  to  die  suddenly  in  an  attack  of  fainting.  Such  a  case 
is  described  at  p.  124. 

Palpitation  and  other  Abnoemalities  of  Ehythm. — 
Another  symptom  of  importance  is  rapidity  of  the  heart's 
action,  often  combined  with  ii-regularities  of  rhythm. 

This  symptom  is  of  less  value  than  the  others  given  in 
the  class  of  case  we  are  dealing  with,  and  great  care  must  be 
taken  to  exclude  the  many  causes  other  than  myocardial 
weakness  to  which  this  symptom  may  be  due. 

The  question  of  heart  failure  owing  to  irregularities  of 
rhythm,  heart  block,  &c.,  is  too  large  a  one  to  be  touched  upon 


94  HEART  FAILURE 

here,  although  many  of  the  cases  may  show  early  symptoms 
of  a  distinctive  type. 

The  symptom  of  cyanosis  may  be  of  value,  though  it  occurs 
as  a  late  rather  than  an  early  symptom. 

No  Dropsy. — Dropsy  is  a  symptom  which,  in  such  cases  as 
we  are  now  speaking  of,  is  always  absent.  The  heart  has  not 
strength  enough  to  keep  up  the  venous  plethora  upon  which 
it  depends. 

Its  presence  may  help  to  distinguish  the  cases  in  the  last 
group — namely,  cases  of  strong  heart  without  enlargement — 
from  the  cases  of  weak  heart  of  which  w^e  are  now  speaking. 

Physical  Signs  of  Heart  Failure  in  Weak  Hearts. — The 
main  signs  upon  which  the  diagnosis  of  myocardial  weakness 
is  based  are,  in  later  as  in  earher  life,  those  which  show  that  less 
than  the  normal  amount  of  blood  is  being  kept  in  active 
circulation  by  the  heart.  And  of  these  signs  the  ones  which 
are  due  to  emptiness  of  the  great  veins  and  of  the  blood-vessels 
of  the  thorax  generally  are  by  far  the  most  important. 

The  limiting  effect  which  rigidity  of  the  fibrous  tissues 
has  upon  the  compensatory  rise  in  the  average  level  of  the 
diaphragm  has  already  been  referred  to.  This  interference 
with  its  compensatory  elevation  is  especially  noticeable  on 
the  right  side,  where  the  presence  of  the  liver  further  interferes 
with  its  movement.  So  much  is  this  the  case  that  in  the  latter 
half  of  life  it  is  not  at  all  common  to  detect  any  elevation  of 
the  right  half  of  the  diaphragm  as  a  result  of  cardiac  failure. 

On  the  left  side  the  diaphragm  is  more  free  to  move,  and 
the  level  of  the  gastric  resonance,  as  the  patient  lies  on  his 
back,  is  a  very  important  guide  to  the  amount  of  blood  that 
is  being  kept  in  circulation  in  the  thorax. 

The  occm-rence  of  full  gastric  resonance  in  the  fifth  inter- 
space is  extremely  suggestive  of  cardiac  weakness. 

Of  almost  equal  importance  with  the  change  in  the  gastric 
resonance  is  the  degree  of  hoUowing  or  fullness  of  the  supra- 
clavicular spaces. 

It  is  probable  that  in  later  life  these  spaces  form  a  more 
useful  guide  than  in  earlier  life ;  for  in  early  life  the  ready 
yielding  of  the  diaphragm,  owing  to  the  softness  and  elasticity 
of  its  fibrous  tissues,  will  lessen  the  tendency  to  in-drawing 


WITHOUT  ENLARGEMENT  95 

of  the  tissues  above  the  clavicle,  whereas  in  later  life  the  greater 
rigidity  of  its  fibrous  tissues  will  tend  to  accentuate  that 
hollowing  by  hmiting  the  compensatory  movements  of  the 
floor  of  the  thorax. 

Certain  it  is  that  the  careful  and  systematic  study  of  the 
conditions  observable  at  the  root  of  the  neck  do  give  very 
valuable  information  as  to  slight  changes  in  the  heart's  activity 
{vide  p.  134). 

It  is  also  of  importance  to  note  the  condition  of  the  veins 
above  the  level  of  the  clavicle,  although  in  the  cases  now  dealt 
with  they  are  usually  not  distended.  Emptiness  of  the  neck 
veins  is  characteristic  of  great  myocardial  weakness.  A  fm'ther 
discussion  of  the  venous  phenomena  of  cardiac  failure  will  be 
found  at  p.  132. 

The  size  of  the  absolute  dullness  of  the  liver,  as  the  patient 
lies  in  bed,  also  gives  very  valuable  information  as  to  the  degree 
of  fullness  which  the  heart  is  able  to  maintain  in  the  blood- 
vessels. 

For  even  in  later  hfe — apart  from  such  conditions  as 
cirrhosis — the  liver  commonly  seems  to  retain  sufficient 
elasticity  to  show  changes  in  the  size  of  its  area  of  absolute 
dullness  when  less  distended  with  blood  than  normal ;  and  in 
a  case  of  myocardial  weakness  the  variations  in  the  position 
of  the  lower  border  of  its  absolute  dullness  are  found  to  coincide 
with  the  variations  in  the  strength  of  the  heart. 

The  stronger  the  heart  the  lower  the  level,  and  the  weaker 
the  heart  the  higher  will  it  be. 

Quite  late  in  life,  however,  one  would  not  expect  to  see 
the  extreme  degrees  of  disappearance  of  the  absolute  dullness 
which  are  seen  earlier  in  life. 

Also  on  the  left  side  the  disappearance  of  the  dullness 
of  the  left  lobe  of  the  liver  is  a  very  useful  sign  of  heart 
failure. 

As  regards  the  pulse  there  is  not  much  to  be  said  ;  for, 
although  when  weak  and  small  it  gives  very  valuable  evidence, 
when,  on  the  other  hand,  it  appears  to  be  good  it  is  a  very  un- 
certain guide  ;  for,  unless  the  usual  character  of  the  pulse  is 
known,  it  is  very  difficult  to  say  on  first  feehng  a  pulse  whether 
there  is  anything  about  it  to  indicate  heart  failure. 


96  HEART  FAILURE 

The  interpretation  of  the  pulse  in  later  Ufe  is  very  difficult 
and  complex,  and  it  is  further  discussed  at  p.  143. 

And  now  as  to  the  physical  signs  of  severe  heart  failui-e 
that  may  be  obtained  from  the  examination  of  the  heart  itself. 

When  the  heart  is  not  very  rigid,  we  may  find — just  as  is 
the  case  earher  in  hfe  : — 

Diminution  in  the  area  of  cardiac  dullness,  and  especially 
a  raising  of  its  lower  border  from  rise  of  the  diaphragm  ; 
a  weak  or  absent  cardiac  impulse  is  also  of  value. 

Auscultation. — With  regard  to  the  heart  sounds,  the 
following  points  are  of  importance.  In  addition  to  their 
being  simply  w^eak,  they  are  often  also  short,  and  do  not  give 
the  impression  of  being  produced  by  a  properly  vigorous 
contraction  of  the  heart.  Another  important  fact  may  be 
noticeable — namely,  that  in  spite  of  the  dyspnoea  and  the 
certainly  existing  embarrassment  of  the  pulmonary  cnculation, 
there  is  httle  or  no  increase  in  the  loudness  of  the  pulmonary 
second  sound  or  of  the  first  sound  audible  over  the  right 
ventricle. 

The  absence  of  right  ventricular  pulsation  and  also  of 
accentuation  of  the  right  ventricular  sounds,  in  spite  of  the 
presence  of  distinct  cardiac  dyspnoea,  may  be  taken  as  almost 
certain  evidence  of  muscular  weakness  of  the  right  ventricle. 

WTien,  in  addition  to  this,  it  is  found  that  the  absolute  cardiac 
dullness  does  not  reach  as  far  to  the  right  as  the  edge  of  the 
sternum,  but  that  resonance  (due  to  the  right  lung  over- 
lapping the  heart)  is  found  at  the  sternal  ends  of  the  fom'th 
and  fifth  left  interspaces,  the  evidences  in  favour  of  a  small 
weak  right  ventricle  are  very  strong  indeed. 

If  the  importance  of  the  diagnostic  points  here  referred 
to  was  more  generally  recognised  and  more  often  looked  for 
in  doubtful  cases  of  heart  weakness  in  later  hfe,  the  result 
would  be  that  fewer  cases  of  dangerous  myocardial  weakness 
would  be  missed,  and  fewer  people  would  die  sudden  deaths 
from  heart  failure  for  want  of  warning  as  to  what  was  safe 
for  them  to  do  and  what  was  not. 

In  the  more  rigid  type  of  heart  most  of  these  evidences 
of  failure  may  not  be  observable,  except  the  absence  of  cardiac 


WITHOUT  ENLARGEMENT  97 

impulse  and  the  weak  heart  sounds  ;  and,  if  the  patient  is  fairly- 
fat,  we  may  not  be  able  to  lay  much  stress  on  these. 

Nevertheless,  as  a  rule  in  later  life,  we  are  able  to  be  fairly 
certain  of  the  presence  of  myocardial  weakness  when  we  find 
heart  failure  associated  with  the  following  : — 

Absence  of  venous  plethora,  as  shown  by  empty  neck 
veins  and  hollowing  above  the  clavicle. 

Weak  or  impalpable  jugular  bulb  pulsation. 

Gastric  resonance  higher  than  normal,  especially  if  well 
into  the  fifth  left  interspace. 

Smallness  of  the  absolute  liver  dullness  especially  if  it 
do  not  reach  as  low  as  the  costal  arch,  and  if  the  dullness 
of  the  left  lobe  be  nearly  or  quite  absent. 

Diminution  in  the  size  of  the  area  of  cardiac  dullness,  with 
absence  of  the  cardiac  impulse  and  heart  sounds  weaker  than 
normal. 

In  illustration  of  these  points,  the  following  clinical  history 
is  given,  and  the  diagrams  of  the  chest  show  clearly  from  day 
to  day  how  these  signs  varied  in  a  manner  distinctly  suggestive 
of  their  reliability. 

Heart  Failure  without  Enlargement  Complicating 
Pneumonia 

The  following  case  illustrates  well  the  importance  of  re- 
cognising the  signs  of  myocardial  weakness  of  which  we  have 
just  been  speaking  : — • 

The  patient  was  a  man  about  forty,  who  was  suffering  from 
pneumonia  of  the  right  lower  lobe,  with  some  signs  that  the  left 
lower  lobe  was  also  about  to  become  involved.  He  had  been 
only  two  days  ill,  and  in  spite  of  the  severity  of  the  local  changes 
the  temperature  was  only  about  101°  F.,  and  the  pulse  about 
100,  occasionally  rising  to  110.  The  respirations,  on  the  other 
hand,  were  fifty  per  minute,  though  this  might  partly  be 
accounted  for  by  the  presence  of  a  good  deal  of  pleuritic  pain. 

There  was  very  little  cyanosis,  although  several  times 
during  the  last  twenty-four  hours  the  patient  had  been  decidedly 
blue. 


98  HEAKT  FAILUKE 

The  examination  of  the  heart  showed  a  condition  that  was 
not  at  all  typical  of  so  severe  a  case  of  pneumonia. 

There  was  no  cardiac  dilatation,  and  the  cardiac  impulse  was 
almost  imperceptible. 

There  was  no  absolute  cardiac  dullness,  and  only  a  little  rela- 
tive dullness  in  the  third  interspace,  and  about  two  inches  in  the 
fourth.  In  the  fifth  interspace  there  was  full  gastric  resonance 
up  to  the  lower  border  of  the  fifth  rib. 

There  was  no  absolute  liver  dullness  in  the  middle  line,  but 
the  full  gastric  resonance  did  not  reach  higher  than  about  the 
tip  of  the  xiphoid  cartilage.  The  absolute  dullness  of  the  right 
lobe  of  the  liver  was  also  small  and  barely  reached  down  to  the 
costal  arch  and  did  not  come  to  within  an  inch  or  more  of  the 
middle  line. 

The  veins  of  the  neck  were  not  at  all  distended,  nor  was  the 
hollow  above  the  clavicles  filled  up.  There  was  slight  visible 
pulsation  in  the  neck  veins,  but  it  was  too  feeble  to  be  palpable, 
and  the  pulsation  of  the  jugular  bulb  was  also  too  feeble  to  be 
readily  distinguished  by  the  finger. 

All  the  cardiac  sounds  were  weaker  than  normal,  and  those 
over  the  right  ventricle  were  slightly  better  marked  than  those 
over  the  left  (see  fig.  7). 

Here,  then,  was  a  case  where  a  very  considerable  degree  of 
interference  with  the  pulmonary  circulation  was  unaccompanied 
by  any  distinct  signs  of  venous  plethora  or  of  overaction  of 
the  right  ventricle.  Moreover,  in  spite  of  nearly  the  whole 
of  the  lower  lobe  of  the  right  lung  being  functionally  inactive 
there  was  not  any  increase  in  the  size  or  activity  of  the  left 
lung  and  there  was,  on  the  other  hand,  an  actual  diminution 
in  the  cubic  content  of  the  left  side  of  the  chest,  as  proved 
by  the  fact  that  the  diaphragm  was  1  inch  or  H  inch 
higher  than  normal  on  that  side. 

The  marked  rise  in  the  level  of  the  gastric  resonance  proved 
this  to  be  the  case. 

Had  the  level  of  the  gastric  resonance  and  the  size  of  the 
liver  dullness  not  been  looked  for,  the  severity  of  the  case 
might  very  easily  have  been  overlooked.  One  might  easily 
have  given  a  very  good  prognosis,  saying  : — 

'  It  is  quite  evident  that  the  amount  of  damage  to  the 
lung  is  much  less  than  the  physical  signs  v/ould  lead  us  to 


WITHOUT  ENLARGEMENT  99 

believe,  for  the  heart  is  not  at  all  affected  by  it  ;  there  is  no 
fullness  of  the  veins,  and  there  are  no  signs  that  any  extra 
strain  is  being  thrown  on  the  right  ventricle — as  evidenced 
by  the  absence  of  pulsation  and  there  being  no  accentuation 
of  the  pulmonary  and  tricuspid  sounds.  The  heart  sounds 
at  the  apex  are  certainly  rather  weak,  and  the  area  of  cardiac 
dullness  not  quite  as  extensive  as  normal — but  this  is  easily 
explained  by  a  compensatory  enlargement  of  the  left  lung.' 

In  the  light  of  what  has  been  already  said,  the  incorrectness 
of  such  an  interpretation  of  the  cardiac  condition  is  manifest. 

The  case  is  really  one  of  severe  and  dangerous  myocardial 
weakness,  and  the  further  history  of  the  case  helps  to  explain 
the  cause  of  the  condition.  Three  weeks  prior  to  the  present 
attack,  he  had  an  influenzal  attack  accompanied  by  severe 
pains  in  back  and  limbs  which  kept  him  in  the  house  ten  days, 
seven  of  which  were  spent  in  bed.  During  the  next  ten  daysj 
he  did  his  work  in  spite  of  great  weariness  and  exhaustion. 

This  weariness  probably  meant  that  some  myocardial 
weakness  resulted  from  his  influenza-like  attack,  and  the 
toxins  of  his  pneumonia  attack  had  still  further  poisoned 
the  heart  muscle,  thus  bringing  about  the  smallness  and 
feebleness  of  the  heart  and  the  rise  of  the  diaphragm  which 
accompanied  it. 

The  importance  of  the  recognition  of  this  fact  is  great  ; 
for  the  danger  of  over-stimulating  such  a  heart  with  digitalis 
would  be  very  considerable.  The  immediate  and  the  distant 
prognosis,  too,  are  very  different  from  those  of  a  simple  case 
of  pneumonia.  The  risk  to  life  is  gi'eater ;  and  if  this  be  sur- 
mounted, the  cardiac  weakness  would  in  all  probability  prevent 
his  returning  to  work  for  months  rather  than  weeks  after 
his  recovery  from  the  pneumonia. 

What  has  just  been  said  about  this  case  was  written  on 
the  evening  after  the  patient  was  first  seen,  and  its  correctness 
was  proved  by  the  fm-ther  progi-ess  of  the  case  which  is  here 
given,  and  the  extreme  weakness  of  the  heart  was  shown  by 
the  fact  that  on  the  seventh  day  of  his  illness,  when  apparently 
going  on  quite  well,  a  fairly  severe  attack  of  coughing  nearly 
caused  his  death,  for  he  became  extremely  cyanosed  and 
pulseless,  and  appeared  to  be  dying.     He  responded,  however, 

H  2 


A  Case  of  Sevebe  Pneumonia  with  Myocardial  Weakness,  where  Variations 
IN  THE  Cardiac  Strength  were  shown  by  Daily  Variations  in  the  Size  of  the 
Cardiac  and  Liver  Dullness  and  in  the  Level  of  the  Diaphragm 


■space 


Fig.  7. 

Wmiam  H.,  aged  forty,  March  15,  1913. 
Extensive  pneumonia  of  right  lung.  Kote  the 
high  level  of  the  gastric  resonance  showing  diminu- 
tion of  the  healthy  left  lung  instead  of  the  usual 
compensatory  enlargement.  Xote  also  the  small- 
ness  of  the  heart  instead  of  the  dilatation  usual  in 
severe  pneumonia.  These  and  other  signs  of 
lessened  volume  of  the  blood  in  circulation  show 
the  presence  of  dangerous  myocardial  weakness. 


Fig.  8. 

WiUiam  H.,  March  19  (i.e.  four  days 
later).  Cardiac  and  Uver  dullness  increased, 
diaphragm  less  liigh  on  the  left  side,  and 
other  signs  of  increasing  heart  strength. 


i 


I 


in  ^^^jspdce 


Fig.  9. 

William  H.,  March  20.  Increase  of  liver  dullness. 
Onset  of  right  pleural  effusion. 


Fig.  10. 

William  H.,  March  21.  Less  cardiac  dilata- 
tion. More  pleuritic  effusion  and  more  consoli- 
dation of  right  lung. 


Fig 


William  H.,  March  22.  Commenciug  ab- 
sorption of  pleuritic  effusion  and  lessening  of 
liver  dullness  from  a  rise  of  the  diapliragm. 


ElG 


WilUam  H.,  March  24.  Further  absorption 
of  the  pleuritic  effusion.  Lessened  liver  dull- 
ness, probably  from  rise  of  right  diaphragm. 
Sudden  rise  of  blood  pressure  from  110  to  130, 
due  to  absorjjtion  of  toxins  from  pleura,  lead 
to  some  enlargement  of  the  right  ventricle. 


Fig.  13. 

WiUiam  H.,  March  25.  Diminished  cardiac 
and  liver  dullness.  Blood  pressure  down  to 
126  mm.  of  mercury.  Left  ventricle  a  Uttle 
larger.    Eight  ventricle  smaller  again. 


Fig.  U. 

WiUiam  H.,  March  27.  Heart  rather 
stronger  and  larger.  Increase  of  dullness 
on  the  right  is  due  to  a  return  of  the 
pleural  effusion. 


102  HEART  FAILURE 

to  free  stimulation  and  to  ether  subcutaneously,  and  when 
the  pulse  returned  it  was  found  to  be  148  per  minute. 

The  case  is  so  instructive  that  a  series  of  diagrams  of  the 
changes  in  the  physical  signs  from  da}'  to  day,  with  short 
explanatory  notes,  are  here  given. 

The  further  progress  of  this  case  is  of  great  interest  also  in 
connection  with  the  diagnostic  point  of  which  we  are  now 
speaking. 

Paintness  and  weakness  were  the  main  features  of  his  ill- 
ness ;  he  had  not  the  restlessness  and  distress  of  an  ordinary 
pneumonia. 

During  the  next  four  or  five  days,  he  distinctly  improved  ; 
the  apex  beat  reappeared,  and  in  three  days  had  become  well 
localised  and  fairly  strong  ;  the  liver  dullness  had  returned  and 
was  just  at  or  below  the  costal  arch,  and  the  full  gastric 
resonance  was  at  the  upper  border  of  the  sixth  rib,  although 
there  was  still  some  resonance  to  be  detected  in  the  fifth 
interspace  (see  figs.  8,  9,  and  10). 

Another  interesting  point  was  the  increase  of  relative 
dullness  in  the  third  left  interspace,  showdng  that  the  heart 
was  now  strong  enough  to  cause  some  dilatation  upwards 
of  its  anterior  wall.  The  apex  at  the  same  time  was  less 
far  out. 

Together  with  this  manifest  strengthening  of  the  heart 
there  was  an  increase  in  the  area  of  the  pneumonia.  It  first 
involved  the  middle  lobe  on  the  right  side  and  then  the  lower 
and  outer  part  of  the  upper  lobe. 

Next  day,  the  eleventh  day  of  his  illness,  he  was  not  so  well. 
The  condition  of  the  heart  and  fiver  suggested  a  loss  instead  of 
a  gain  in  cardiac  strength,  for  the  absolute  liver  dullness  was  now 
half  an  inch  above  the  costal  arch,  and  the  absolute  cardiac 
dullness  had  gone  ;  the  blood  pressure,  moreover,  had  dropped 
from  118  mm.  to  110  mm.  (see  fig.  11). 

The  condition  of  the  lung  posteriorly  suggested  a  pleural 
effusion,  and  a  puncture  showed  clear  serum  with  flakes  of  lymph 
and  abundance  of  pneumococci. 

Two  days  later,  there  was  a  marked  change  in  the  physical 
signs,  although  the  patient  was  shghtly  better  on  the  whole. 

The  liver  dullness,  while  good  in  the  region  of  the  xiphoid 
cartilage,  was  much  less  marked  below  the  seventh  rib ;  and  next 


WITHOUT  ENLARGEMENT 


103 


day  there  was  full  intestinal  resonance  below  the  seventh  rib 
internal  to  the  nipple  hne,  and  the  anterior  margin  of  the  area 
of  absolute  dullness  was  three  inches  away  from  the  costal  arch 
and  parallel  to  it ;  the  cardiac  dullness,  too,  was  less  and  the 
relative  dullness  not  reaching  above  the  fourth  rib.  On  the 
other  hand,  the  heart  was  much  stronger,  the  apical  fii'st 
sound  being  if  anything  louder  than  normal,  and  the  right 
ventricular  sound  also  good  though  not  so  loud.  The  pulse, 
too,  was  stronger,  and  the  blood  pressure  138  mm.  (see  fig.  12). 

The  explanation  of  these  changes  was  given  by  examination 
of  the  lung  ;  for  not  only  had  the  dullness  diminished  anteriorly, 
as  shown  in  the  diagram,  but 
on  examining  the  back  it  was 
found  that,  instead  of  the 
dullness  of  the  right  side 
reaching  to  the  middle  line, 
or  even  crossing  it  towards 
the  base  of  the  lung,  the  whole 
of  the  spine  was  now  resonant 
up  to  the  level  of  the  angle  of 
the  scapular  ;  while  above  this 
level  there  was  a  band  of 
resonance  one  inch  wide  to 
right  of  the  spine,  over  which 
breath  sounds,  similar  to 
those  of  the  left  lung,  were 
audible. 

There  was  no  doubt  that 
a  considerable  amount  of 
serum  had  been  rapidly  ab- 
sorbed from  the  pleura  and,  owing  to  the  consoHdation 
of  the  lung  preventing  its  expansion,  compensatory  en- 
largement of  the  other  Imig  had  taken  place  and  the 
diaphragm  also  had  risen,  thus  lessening  the  amount  of  hver 
tissue  left  in  contact  with  the  lower  ribs.  The  fact  that  the 
heart  had  not  shifted  towards  the  right,  as  well  as  the  greater 
degree  of  crossing  of  the  left  lung  posteriorly  being  above,  m- 
stead  of  below,  the  level  of  the  angle  of  the  scapular,  was 
exphcable  on  the  gi-ound  of  the  rigidity  and  possible  adhesions 
of  the  affected  right  lower  and  middle  lobes. 

This  theory  of  the  absorption  of  the  pleural  fluid  wth  its 
contained   pneumococcal   toxins   was   also   suggested    by  the 


Fig.  15. 

William  H.,  ilarcli  29.  Heart  stronger 
and  larger.  Left  ventricle  dilated  now,  but 
pleural  dullness  increased. 


104  HEART  FAILURE 

subsequent  rise  in  the  patient's  temperature,  his  hot,  dry  skin, 
and  also  the  sudden  rise  in  the  blood  pressure. 

My  experience  during  the  last  twelve  months  has  seemed 
to  show  that  unrecognised  pneumococcal  infection — such  as  in 
frontal  sinus  empyema — ^is  sometimes  the  cause  of  high  blood 
pressure,  and  ordinary  pneumococcal  infection  seems  to  have 
a  special  effect  upon  the  pulse.  The  movement  of  the  blood 
pressure  in  this  case  was  certainly  very  striking — namely, 
steady  at  118  mm.  of  mercury  from  the  seventeenth  till  the 
twenty-first  of  March  :  110  on  the  twenty-second  ;  then  on  the 
twenty-fourth,  signs  that  the  serum  had  been  absorbed  with 
a  blood  pressure  of  138  ;  very  vigorous  cardiac  pulsation  and 
sounds,  with  strong  venous  pulse  and  fuller  veins. 

Next  day,  blood  pressure  126  mm.,  followed  in  twenty-four 
hours  by  one  of  120  mm. ;  but  on  this  day  evidence  for  the 
first  time  that  the  left  ventricle  was  beginning  to  enlarge 
a  little,  the  apex  being  4|-  inches  from  the  sternum  and 
palpable  in  the  fifth  interspace,  w^hen  the  ribs  were  elevated 
during  inspiration,  and  in  the  fourth  during  expiration  (see 
figs.  13,  14,  and  15). 

Subsequently,  a  small  localised  empyema  formed  at  the 
right  base,  and  was  opened,  and  then  a  part  of  the  consolidated 
lung  broke  down  and  suppurated  instead  of  resolving. 

The  case  illustrates  the  value  of  careful  percussion  of  the 
heart  and  liver  in  estimating  changes  in  the  heart  and 
chest. 

The  foregoing  is  but  an  illustration.  Any  case  of  heart  failure 
due  to  influenza  or  rheumatism  will  show^  just  as  concise  a 
picture  as  this  or  as  that  given  at  p.  196,  and  the  certainty 
gained  as  to  the  condition  of  the  heart  well  repays  the  few 
minutes  necessary  for  the  exact  and  careful  mapping  out  by 
percussion  of  the  area  of  absolute  and  relative  dullness  in  the 
case  of  both  the  heart  and  liver. 

This  case  also  shows  a  trace  (the  man  %vas  forty-two  years  of 
age)  of  the  dilatation  of  the  anterior  wall  of  the  right  ventricle, 
w^hich  is  spoken  of  as  one  of  the  most  certain  signs  of  the 
retm-n  of  strength  after  a  myocardial  affection  where  the  heart 
is  sufficiently  distensible. 

The  disappearance  of  the  lower  half  of  the  liver  dullness, 


WITHOUT  ENLARGEMENT  105 

owing  to  the  rise  of  the  diaphragm,  is  also  a  good  illustration 
of  this  phenomenon. 

The  following  case  also  illustrates  the  fact  that  myocardial 
weakness,  with  or  without  the  relative  cardiac  rigidity  of 
later  life,  gives  a  different  picture  in  the  case  of  pneumonia 
from  that  afforded  by  a  patient  with  a  strong  heart  in  early 
life. 

In  this  latter  case,  we  can  rely  upon  the  loudness  of  the 
right  ventricular  sounds,  the  amount  of  cardiac  pulsation 
over  the  right  ventricle,  together  with  the  degree  of  fullness 
of  the  veins  and  the  amount  of  pulsation  in  them,  as  indicating 
in  a  reliable  manner  the  degree  in  which  the  pneumonia  is 
interfering  with  the  circulation  and  as  showing  the  severity 
of  the  case. 

Thus,  supposing  we  are  dealing  with  an  influenzal  or  a 
catarrhal  case,  where  there  is  some  tubular  breathing  over 
the  lower  lobe  of  the  right  lung  with  weak  and  wheezy  breathing 
and  some  slight  impairment  of  the  percussion  note  at  the 
left  base,  combined  with  a  quietly  acting  heart  showing  neither 
dilatation  of  the  right  ventricle  nor  any  evidence  of  its  failure, 
by  fullness  or  pulsation  of  the  neck  veins,  we  should  be  inclined 
to  say  that  the  pneumonia  was  not  of  a  very  serious  type,  and 
that  the  prognosis  was  good.  If  we  were  dealing  with  a  young 
and  fairly  strong  patient,  this  diagnosis  would  probably  be 
correct.  If,  on  the  other  hand,  the  patient  was  well  past  middle 
life,  we  might  be  making  a  dangerous  mistake  by  reading  the 
symptoms  thus. 

Here  is  such  a  case.  An  elderly  lady  suddenly  developed 
a  severe  feverish  cold  with  bronchitic  symptoms.  On  the 
second  day  signs  of  influenzal  pulmonary  catarrh  were  present. 
On  the  fourth  day  the  following  condition  was  present.  There 
was  some  consolidation  with  nearly  tubular  breathing  along 
the  upper  border  of  the  right  lower  lobe  posteriorly.  Over  the 
greater  part  of  the  left  lower  lobe,  posteriorly,  the  breath  sounds 
were  weak  and  wheezy  and  the  resonance  a  little  impaired.  As 
to  the  heart,  there  was  no  increase  in  the  loudness  of  the  right 
ventricular  sounds,  and  there  was  no  pulsation  over  the  right 
ventricle,  visible  or  palpable,  and  no  signs  of  dilatation,  and 
the  condition  of  the  right  ventricle  was  much  the  same  as  it 


106  HEART  FAILURE 

was  before  the  attack.  There  was  no  increased  fulhiess  of  the 
neck  veins,  and  Httle,  if  any,  pulsation — ^just  as  was  the  case 
prior  to  the  attack.  The  pulse  was,  however,  bad,  and  the  left 
ventricle  more  dilated  than  was  usual  with  the  patient.  Now, 
how  were  these  signs  to  be  interpreted  ?  Did  this  quietly 
acting  right  ventricle  imply  that  the  pneumonia  was  only 
slightly  interfering  with  the  circulation  through  the  lungs  and 
that  the  right  ventricle  was  in  a  satisfactory  condition  ?  By  no 
means.  Had  I  not  known  what  the  usual  loudness  of  the  right 
ventricular  sounds  were,  I  might  possibly  have  been  deceived 
and  taken  this  view ;  but  as  it  was,  the  recognition  of  the  fact 
that  the  right  ventricular  sounds  were  rather  less  loud  than 
was  usual  in  this  patient,  showed  what  was  really  taking  place 
— namely,  that  the  pulmonary  circulation  was  so  embarrassed 
that  the  somewhat  feeble  right  ventricle  could  not  cope  with  it, 
and  there  was  a  great  risk  of  fatal  dyspnoea.  This  was  shown 
also  by  an  alarming  attack  of  breathlessness  which  followed 
upon  some  slight  undue  exertion  early  on  in  the  illness.  It  was 
also  proved  by  the  fact  that  when  the  lung  began  to  clear,  the 
right  ventricle  became  stronger  again,  and  its. sounds  were  louder 
and  pulsation  became  evident  just  to  the  left  of  the  sternum. 
The  mode  of  resolution  proved  as  was  suspected — that  the 
affection  of  the  left  lung  was  really  a  central  consolidation  with 
blocking  of  the  bronchi ;  for,  as  resolution  proceeded,  a  certain 
amount  of  faint  tubular  breathing  became  audible,  and  the 
whispered  voice  sound  was  far  too  audible  over  much  of  the 
lower  lobe  {vide  p.  140). 

In  such  a  case  as  this  a  misreading  of  the  heart  condition 
early  on  might  have  easily  led  to  a  fatal  result,  through 
allowing  the  patient  to  attempt  exertion — such  as  getting  out 
of  bed. 

Difficulties  in  diagnosis  may  arise  in  cases  where,  in  later 
life,  myocardial  weakness  from  muscular  degeneration  or  from 
the  toxins  of  infective  disease  occurs  in  a  heart  already  enlarged 
from  valvular  disease  and  overstrain.  But  here  the  general 
principle  of  looking  for  signs  of  lessened  vigour,  and  that  the 
heart  is  not  able  to  keep  in  circulation  the  amount  of  blood 
that  it  has  been  in  the  habit  of  doing,  is  just  as  reliable  as  it 
was  in  the  cases  already  described,  where  there  was  an  onset 
of  muscular  failure  in  a  heart  that  was  previously  normal. 

A  lessening  in  the  loudness  of  the  murmurs,  a  diminution 


WITHOUT  ENLARGEMENT  107 

in  the  vigour  of  the  venous  pulsation  in  the  neck  and  of  the 
size  of  the  enlarged  hver,  would  all  point  to  the  onset  of 
myocardial  weakness. 

In  order  to  illustrate  further  the  difference  between  cases 
of  heart  failure  with  enlargement,  and  heart  failure  without 
enlargement,  the  two  following  clinical  pictures  are  given: — 

The  two  patients  here  referred  to  were  both  seen  on  the 
same  morning  and  in  consultation  with  the  same  doctor. 

Both  were  ladies  over  eighty,  and  both  were  hindered  by 
breathlessness  and  weakness  from  taking  much  exercise.  The 
elder  of  the  two,  a  lady  of  eighty-live,  was  vigorous  in  mind  and 
body  for  her  age,  and  able  to  go  upstairs  and  do  a  certain  amount 
of  walking  on  the  level,  but  any  exceeding  of  the  narrow  hmits 
which  were  set  her  was  sure  to  produce  exhaustion  and  some 
dyspnoea. 

In  this  case  the  heart  showed  what  may  be  called  the  ordi- 
nary signs  of  heart  failure  with  enlargement.  The  apex  was  in 
the  sixth  space,  5|  inches  from  the  middle  Une,  i.e.  close  to  the 
anterior  axillary  hne.  Its  impulse  was  weU  defined,  and  fairly 
well  locahsed.  The  right  ventricle,  too,  was  strong,  and  its 
impulse  would  show  clearly  in  the  fourth  and  fifth  interspaces, 
near  the  sternum,  on  any  overtasking  of  the  patient's  strength. 
There  was  a  well-marked  but  not  very  loud  mitral  systolic 
murmur,  and  a  loud  superior  vena  cava  murmur  heard  to  the 
right  of  the  sternum  up  to  the  aortic  area. 

The  neck  veins  were  not  distended,  but  pulsation  was  fairly 
well  marked  in  the  jugular  bulb. 

The  pulse  was  full  and  strong — too  full  between  the  beats — 
and  suggestive  of  arterio-sclerosis,  were  it  not  that  the  wall  was 
soft  and  of  good  elasticity.  The  heart  rhythm  was  at  times 
shghtly  irregular,  owing  to  occasional  extra  systoles  following 
close  on  the  preceding  first  sound,  and  almost  certainly  what 
may  be  called  aspii'ation  extra  systoles,  and  due  to  mechanical 
stimulation  of  the  left  ventricle  by  the  inrush  of  aspirated  blood, 
and  implying  in  this  case  dilatation  of  the  left  auricle  (see 
•p.  497). 

The  blood  pressure  was  170  mm.,  and  the  pulsation  of  the 
mercury  column  markedly  lessened  below  120  mm.,  suggesting 
that  this  was  the  diastohc  pressure. 

This  is  an  ordinary  case  of  heart  failme  with  dilatation 
secondary   to   high   pulse   tension,   and  in   this   patient   the 


108  HEART  FAILURE 

occurrence  of  exhaustion  rather  than  dyspnoea  showed  that 
the  left  ventricle  was  more  faulty  than  the  right  ;  the  same 
fact  was  pointed  to  by  the  occurrence,  wdien  the  patient  over- 
exerted herself,  of  signs  of  increased  right  ventricular  action 
— namely,  the  appearance  of  a  right  ventricular  impulse  and 
an  increase  in  the  loudness  of  the  right  ventricular  sounds. 

In  contrast  with  this  was  the  second  case  seen.  Here  the 
lady  was  also  over  eighty,  and  was  also  active  in  mind  and 
body,  although  for  some  years  past  she  had  been  hindered  by 
marked  dyspnoea  from  any  continuous  or  severe  exertion. 
One-half  or  three-quarters  of  a  mile  on  the  level  was  all  the 
exercise  she  could  take  without  the  occurrence  of  troublesome 
dyspnoea. 

Her  pulse  was  in  marked  contrast  to  the  last  patient's.  It 
was  very  small,  but  regular,  and  there  was  no  marked  diastoHc 
over-fullness  of  the  vessel  as  in  the  other  case,  enabling  the 
artery  to  be  rolled  under  the  finger.  The  blood  pressure  was 
152  mm.  of  mercury,  and  the  diastolic  pressure  was  100. 
There  was  no  pulsation  visible  in  the  neck  veins,  and  there  was 
distinct  hollowing  above  the  clavicles,  suggesting  emptiness  of 
the  veins.  This  was  confirmed  by  palpation  of  the  jugular 
bulb,  for  its  pulsation  was  not  well  marked. 

On  examining  the  heart,  no  pulsation  could  be  detected  any- 
where, and  the  apex  beat  could  not  be  felt.  The  cardiac  dullness, 
too,  was  decidedly  small,  and  the  diaphragm  high,  as  judged  by 
the  level  of  the  gastric  resonance,  which  reached  to  the  fifth 
rib  in  the  left  nipple  line.  The  liver  dullness,  too,  was  much 
smaller  than  normal,  and  well-marked  intestinal  resonance  was 
obtainable,  as  the  patient  lay  in  bed,  for  more  than  one  inch 
above  the  right  costal  arch.  In  the  other  patient  the  Hver 
was  very  nearly  normal  in  size  and  the  gastric  resonance  was 
normal. 

The  heart  sounds  were  weak,  and  there  was  no  murmur 
present. 

An  interesting  feature  about  the  case  was  that  in  spite  of 
the  quietness  of  the  heart's  action  andsounds,and  the  smallness 
of  the  pulse,  the  pulsation  of  the  carotid  arteries  was  strong 
and  vigorous,  much  more  so  than  normal,  and  the  artery  was 
full  and  fairly  hard  throughout  the  diastole,  as  in  cases  of 
arterio-sclerosis. 


WITHOUT  ENLAKGEMENT  109 

The  condition  of  the  carotids,  as  compared  with  the  pulse, 
suggested  the  probabihty  that  the  smallness  of  the  radial 
artery  was  a  compensatory  change  secondary  to  the  cardiac 
weakness,  and  that  with  any  increase  in  the  heart's  strength 
there  would  be  a  marked  increase  in  the  volume  of  the  pulse. 
In  answer  to  this  suggestion,  the  practitioner  in  charge  of  the 
case  said  that  the  improvement  in  the  volume  of  the  pulse  was 
sometimes  remarkable,  and  that  sometimes  the  pulse  was  very 
much  larger  than  it  was  at  the  time  of  examination. 

As  regards  this  case,  it  was  quite  evident  that  of  the  two 
sides  of  the  heart  the  right  ventricle  was  the  weaker,  and  the 
condition  of  the  circulation  pointed  to  a  somewhat  considerable 
amount  of  degeneration  of  the  muscle  of  that  chamber.  The 
next  question  was  whether  this  was  the  only  serious  cause  of 
interference  with  the  heart's  action. 

The  full  and  sustained  carotid  pulse  suggested  the  possi- 
bihty  that  there  was  also  some  rigidity  of  the  first  part  of  the 
aorta,  because  were  the  first  part  of  the  aorta  normal  there  was 
no  reason  in  such  a  case  as  this  for  the  larger  arteries  showing 
more  pulsation  than  normal,  while  the  smaller  ones  showed  less. 
In  spasmodic  contraction  of  the  peripheral  vessels  such  a 
condition  might  be  possible,  but  there  was  no  suggestion  of  this 
here,  as  there  was  no  sign  of  any  faulty  circulation  in  hands  or 
feet.  The  colour  and  warmth  of  hands  and  feet  were  always 
good  and  the  dilatability  of  the  radial  artery  when  the  heart 
was  excited  negatived  the  presence  of  muscular  spasm. 

The  absence  of  any  dilatation  and  hypertrophy  of  the  left 
ventricle — such  as  usually  accompanies  a  loss  of  elasticity  of  the 
first  part  of  the  aorta — would  in  this  case  be  prevented  by  the 
faulty  nutrition  of  the  cardiac  muscle,  and  therefore  weakness 
and  breathlessness  would  advance  pari  passu  with  the  change 
in  the  aorta  and  not  be  warded  off  for  a  time  by  muscular 
hypertrophy. 

Some  other  explanation  might,  however,  be  found  for  this 
phenomenon. 

Of  these  two  cases,  the  first  was  one  of  simple  overstrain 
from  high  arterial  tension  in  a  heart  whose  muscular  tissue  was 
fairly  sound  considering  the  patient's  age,  and  was  able  to  de- 
velop an  intraventricular  pressure  in  excess  of  the  resisting 
power   of  the  weaker  portions   of  the  ventricle  walls,  thus 


no  HEART  FAILURE 

causing  dilatation.  In  this  case  there  was  no  great  risk  of 
sudden  death. 

In  the  second  case,  the  primary  cause  of  the  cardiac  failure 
was  muscular  degeneration  involving  the  right  side  of  the 
heart  to  a  much  greater  extent  than  the  left. 

Whether  previously  there  had  been  any  cause  for  embarrass- 
ment— such  as  high  arterial  tension  or  rigidity  of  the  aorta — it 
was  not  easy  to  say,  as  the  myocardial  weakness  would  prevent 
the  characteristic  signs  from  sho^ving  themselves.  The  small- 
ness  of  the  pulse,  and  the  emptiness  of  the  veins  and  other 
signs  of  a  diminution  in  the  volume  of  blood  in  active  circu- 
lation, were  a  measure  of  the  muscular  feebleness  of  the  heart, 
and  in  this  connection  it  was  an  interesting  fact  that  the  patient 
was  an  extremely  small  eater,  her  daily  output  of  urea  being 
150  to  200  gi-ains  only— as  if  nature  were  calling  for  a  reduction 
in  the  intake  of  proteids  in  order  to  assist  in  keeping  the 
volume  of  the  blood  below  normal. 

The  other  patient  had  a  good  appetite,  and  her  intake  of 
flesh  food  had  to  be  compulsorily  lowered  in  order  to  lessen  her 
pm-in  intake  and  keep  down  the  blood  pressure. 


Early  Diagnosis  of  Heart  Failure  in  Cases  of  Valvular 
Disease  in  Later  Life 

The  same  principles  are  applicable  to  the  recognition  of 
muscular  failure  in  a  heart  that  had  previously  been  enlarged 
afi  a  result  of  valvular  disease  or  overstrain,  as  those  here  laid 
down  for  the  recognition  of  cardiac  failure  in  a  previously 
healthy  heart.  In  a  heart  dilated  and  hypertrophied  from 
either  of  those  causes,  the  onset  of  muscular  failure  would  be 
accompanied  by  a  lessening  in  the  vigour  and  amount  of  the 
venous  pulsation  in  the  neck  and  by  a  lessening  of  the  loudness 
of  the  heart  sounds.  There  might  also  be  a  lessening  in  the 
amount  of  dilatation  of  the  right  ventricle,  and  this  change, 
together  with  the  lessened  pulsation  in  the  neck,  might  very 
readily  be  misinterpreted  and  taken  to  be  a  good  sign  instead 
of  a  very  bad  one. 

A  case  is  mentioned  on  p.  63,  where  a  sudden  diminution 


IN  LATER  LIFE  111 

in  the  size  of  a  distended  liver  was  a  sign  of  sudden  heart  failure 
from  over-stimulation  of  a  weak  and  failing  heart.  Such 
diminution  in  the  size  of  a  liver  enlarged  by  tricuspid  regurgita- 
tion shows  a  lessening  in  the  amount  of  tricuspid  leakage, 
and  might  well  be  due  to  lessened  dilatation  and  recovery  of 
the  ventricle  ;  but  it  must  clearly  be  borne  in  mind  that 
lessened  tricuspid  regurgitation  may  also  be  due  to  the  onset 
of  muscular  weakness,  and  a  sign  of  failure,  and  not  of  a  gain 
in  its  muscular  strength. 

The  changes  described  in  the  case  of  penumonia  on  p.  97 
illustrate  very  well  what  might  be  expected  to  occur  in  a  case 
of  an  overacting  right  ventricle  when,  after  a  time,  muscular 
feebleness  began  to  develop. 

As  the  general  principles  both  of  heart  failure  in  early,  in 
adult,  and  in  later  life  are  fully  applicable  to  these  cases  where 
muscular  weakness  appears  in  a  heart  previously  dilated  or 
hypertrophied  as  a  result  of  valvular  disease  or  overstrain 
the  subject  need  not  be  dealt  ^N-ith  in  greater  detail.  It  is 
hardly  necessary  to  point  out  the  importance  of  early  recog- 
nising muscular  failure  in  cases  of  valvular  disease.  Our 
treatment  of  such  cases  often  has  to  include  powerful 
heart  tonics,  in  order,  for  instance,  to  raise  a  falling  blood 
pressure  up  to  the  level  necessary  for  cardiac  nutrition,  or  in 
other  cases  so  to  raise  the  intraventricular  pressure  that  it 
may  speedily  bring  about  that  dilatation  upon  which  compen- 
sation depends.  In  all  such  cases,  w^e  must  watch  very  closely 
lest  we  go  too  far  and  stimulate  the  heart  to  an  expenditure 
of  energy  which  is  in  excess  of  what  its  powers  of  nutrition 
can  make  good.  The  careful  watching  in  such  cases  for  the 
first  signs  that  the  muscles  of  the  heart  are  becoming  weaker 
from  over-stimulation  is  therefore  of  the  greatest  importance. 
The  early  detection  in  valvular  disease  of  signs  of  muscular 
weakening,  which  disease  of  the  coronary  arteries  slowdy  induces, 
is  also  of  gi-eat  importance  ;  for  a  heart  whose  nutrition  is  not 
good  will  naturally  not  stand  stimulation  as  well  as  one  whose 
nutrition  is  sound. 

Another  case  where  information  of  great  diagnostic 
value  was  gained  from  the  size  of  the  liver  and  heart  is  the 
following  : — 


112  HEART  FAILURE 

A.  H.,  aged  forty-four,  commercial  traveller,  who  used  to  do 
20,000  miles  a  year  in  spite  of  suffering  from  aortic  regurgitation 
of  a  moderate  degi-ee.  When  I  first  saw  him,  he  was  suffering 
from  faihng  compensation  with  a  dilated  right  ventricle, 
breathlessness,  and  pain,  but  no  dropsy.  I  saw  him  again  six 
years  afterwards  and  found  him  to  be  suffering  from  palpita- 
tion and  breathlessness  and  total  inability  to  continue  his 
work — probably  the  result  of  influenza.  On  this  occasion, 
although  his  cardiac  symptoms  w^ere  quite  as  severe  as  when 
seen  six  years  earlier,  the  cardiac  apex  was  not  as  much  outside 
the  nipple  line  by  one  inch,  and  instead  of  there  being  marked 
dilatation  of  the  right  ventricle  the  area  of  cardiac  dullness  was 
quite  small.  Instead  of  the  stomach  level  being  nearly  normal 
(at  the  level  of  the  sixth  rib)  there  were  two  inches  of  gastric 
resonance  in  the  fifth  space.  The  hver  dullness  also  was  small 
in  this  last  attack — not  reaching  the  costal  arch  by  one  inch. 
There  was  no  fullness  of  the  veins  of  the  neck. 

Here  we  are  dealing  with  a  case  of  aortic  regurgitation 
with  breathlessness,  but  without  cardiac  dilatation  or  distension 
of  the  veins.  On  the  other  hand,  there  was  smallness  of  the 
heart,  smallness  of  the  lungs  as  well,  as  judged  by  the  rise 
in  the  gastric  resonance,  although  the  upper  level  of  the  liver 
dullness  was  normal,  and  also  smallness  of  the  Hver  dullness. 

It  was  quite  evident  that  the  man  was  suffering  from  pure 
myocardial  weakness  and  not  the  ordinary  mechanical  failure 
with  a  strong  cardiac  muscle,  which  is  the  usual  cause  of  heart 
failure  in  aortic  regurgitation. 

The  prognosis  for  the  future  was  therefore  much  worse, 
and  the  need  for  cutting  down  his  work  quite  imperative. 
Doubtless,  the  same  estimate  of  his  condition  might  have  been 
arrived  at  without  noting  the  smaUness  of  the  liyer  and  the 
rise  of  the  gastric  resonance  ;  but  these  two  indications  of 
weakened  cnculation  were  of  great  value. 


Short  Notes  upon  some  of  the  Diagnostic  Difficulties 

ASSOCIATED    WITH    THE    RECOGNITION    OF    HeART    FaILURE    IN 

Later  Life. — The  main  cause  of  the  difficulties  which  accom- 
pany the  recognition  of  heart  failm'e  in  later  life  is  to  be 
found    in    the   fact    that   muscular    feebleness  plays  a  very 


DIAGNOSTIC  DIFFICULTIES  113 

important  part  in  that  failure,  and  we  cannot  expect  ttiat 
any  striking  positive  signs — such  as  loud  murmui's,  dilated 
auricles  or  veins,  or  well-marked  pulsations — will  characterise 
feeble  cardiac  action. 

The  physical  signs  of  muscular  failure  must  therefore 
be,  perforce,  negative  in  their  nature.  Consequently,  we  have, 
as  already  pointed  out,  to  rely  much  more  upon  symptoms 
than  upon  positive  signs  for  the  diagnosis  of  this  type  of  heart 
failure  in  later  life.  Symptoms  are,  however,  much  more 
likely  to  be  misleading  than  physical  signs,  owing  to  the 
simulation  of  symptoms  due  to  organic  disease  by  those  due 
merely  to  reflex  disturbances. 

This  section  will  therefore  be  commenced  by  a  few  notes 
upon  the  various  symptoms,  and  with  illustrations  of  some 
of  the  errors  in  diagnosis  that  have  to  be  avoided. 

But  here  a  word  of  apology  must  be  offered  for  fear  any- 
thing approaching  completeness  be  expected  in  the  following 
pages.  The  subject  dealt  mth  is  so  complex  and  so  difficult, 
and  our  knowledge  in  many  respects  so  limited,  that  nothing 
approaching  completeness  or  scientific  method  can  be  attempted 
by  the  writer.  He  can,  at  most,  give  some  illustrations  gathered 
from  his  own  experience  of  some  of  the  pitfalls  into  which  the 
practitioner  and  the  specialist  may  fall  when  face  to  face 
with  cases  of  heart  failm-e,  or  of  supposed  heart  failure,  in 
later  fife. 

There  is  plenty  of  scope  for  a  whole  book  being  written 
upon  this  one  subject  alone. 

Dyspnoea 

Firstly,  as  to  dyspnoea — for  this  sign  is  our  sheet-anchor 
in  dealing  with  cardiac  failure  in  later  life. 

It  is  hardly  necessary  to  point  out  the  necessity  for  making 
certain  that  the  breathlessness  is  of  true  cardiac  origin,  and 
not  due  to  damage  to  the  lungs— an  error  that  can  easily  be 
made  by  any  of  us  from  imperfect  observation  in  a  case  when 
our  attention  is  absorbed  by  some  apparently  obvious  cardiac 
abnormahty  {vide  the  case  described  on  p.  374).  Upon  another 
point    we    must    convince    om-selves — namely     whether    the 

X 


Ill  LATER  LIFE 

dyspnoea,  although  certainly  cardiac  in  origin,  is  or  is  not 
secondary  to  tachycardia,  or,  in  common  parlance,  *  palpitation.' 
In  other  words,  ascertain  whether  the  breathlessness  is  a 
constant  symptom,  or  whether  at  times  it  is  much  less  trouble- 
some than  it  is  at  others.  In  the  latter  case  it  may  be  simply 
secondary  to  a  palpitation  of  reflex  origin,  as  in  the  case  described 
on  p.  115. 

Again,  if  the  dyspnoea  be  a  constant  phenomenon  it  may 
yet  be  associated  with  a  tachycardia — such  as  that  symptomatic . 
of  Graves's  disease,  or  due  to  some  other  cause,  and  not  directly 
due  to  organic  cardiac  failure. 

A  case  may,  however,  occasionally  be  met  with  where  the 
tachycardia  and  its  accompanying  dyspnoea  may  both  be 
associated  with  overstrain,  and  may  represent  organic  damage 
to  the  heart.     Such  a  case  is  given  at  p.  324. 

Dyspnoea  when  a  prominent  symptom  suggests  myocardial 
failure  of  the  right  rather  than  of  the  left  ventricle,  see  p.  154. 

Palpitation 

Another  important  sign  of  heart  weakness  is  palpitation, 
although  it  is  very  commonly  in  later  life  associated  with 
causes  other  than  organic  disease— such  for  instance  as  Graves's 
disease  and  reflex  disturbances.  Moreover,  in  pure  muscular 
failure  the  rapid  conscious  overaction  of  the  heart,  which  patients 
call  palpitation,  is  not  a  very  characteristic  phenomenon. 

Often  associated  with  palpitation  are  the  many  cases  of 
cardiac  irregularity,  some  of  which  are  due  to  organic  damage 
to  the  heart,  as  in  the  case  of  the  various  types  of  irregularity 
with  which  the  name  of  Sir  James  Mackenzie  will  always 
be  associated,  and  some  of  which  are  purely  functional  in 
origin. 

Into  the  former  group  I  shall  not  enter  here,  as  the  subject 
is  too  large  a  one,  and  is,  moreover,  being  very  fully  dealt 
with  by  very  many  writers  at  the  present  time. 

It  may  be  of  interest,  however,  in  this  connection  to  give 
some  illustrative  cases  :  in  one  of  which,  at  all  events,  an  error 
in  diagnosis  might  well  have  been  made,  had  the  patient 
been  a  dozen  years  older. 


PALPITATION  115 

Mr.  W.,  aged  about  forty,  a  dental  practitioner,  came  to  me 
comi^laimng  of  extreme  cardiac  discomfort,  with  a  most  trying 
sense  of  impending  death.  The  heart  was  ahnost  continuously 
irregular,  and  at  times  when  walking  or  exerting  himself,  he 
was  seized  with  violent  palpitation  and  irregularity  ;  he  was 
conscious  of  individual  beats  of  the  heart  so  forcible  that  he 
felt  as  if  they  shook  his  whole  chest,  and  these  were  preceded 
or  followed  by  beats  of  extreme  rapidity,  or  by  a  sensation  that 
his  heart  was  stopping  altogether  and  that  he  was  going  to  fall 
dead. 

Careful  examination  of  the  heart,  however,  showed  no  trace 
of  any  abnormality  in  the  size  or  somids  of  either  ventricle  or 
in  the  venous  or  arterial  circulation,  except  the  arythmia 
already  described.  Moreover,  on  testing  the  strength  of  the 
heart  by  making  the  patient  ascend  stairs,  there  were  no  signs 
of  any  failure  in  its  strength,  so  long  as  the  palpitation  was  not 
extreme  at  the  time.     A  good  prognosis  was  therefore  given. 

This  view  of  the  case  was  borne  out  by  the  history,  for, 
although  the  man  paid  me  very  frequent  visits-  for  some 
months  m  order  that  I  might  examine  his  heart  and  reassure 
him  that  he  was  not  going  to  fall  down  dead  in  the  street,  after 
having  had  it  for  many  months  the  palpitation  suddenly 
left  him :  so  suddenly,  in  fact,  that  he  could  point  to  the  spot 
where  he  was  when  the  sensation  came  over  him  that  his 
palpitation  had  gone  ;  and  strangely  enough  it  happened  as 
he  was  walking  along  the  street  not  two  hundred  yards  from 
my  consulting-rooms. 

The  following  case  also  is  one  which  presented  a  good  deal 
more  difficulty,  and  is  of  very  considerable  interest. 

The  patient  was  a  lady  about  forty  years  of  age,  who  for  two 
years  had  been  working  far  too  hard  in  connection  with  a 
philanthropic  and  rehgious  organisation  in  which  she  was 
interested.  Her  work  involved  physical  as  well  as  nervous 
strain ;  for  she  not  only  conducted  frequent  meetings — speak- 
ing to  various  types  of  audiences — but  also  often  had  long  days 
and  sometimes,  owing  to  absence  of  other  means  of  transport, 
had  herself  to  carry  a  heavy  bag  to  or  from  railway  stations  or 
meetings.  When  she  consulted  me,  her  chief  trouble  consisted 
in  neurasthenic  symptoms  combined  with  most  troublesome 
palpitation  and  breathlessness.     The  history  seemed  to  point 

i2 


116  LATER  LIFE 

to  beurt  weakness,  in  which  nerve  strain  played  an  important 
part,  as  the  cause  of  her  symptoms. 

This  diagnosis  appeared  to  be  confirmed  by  the  examination 
of  the  patient.  She  was  thin.  The  heart  was  rapid  and  the 
pulse  wave  was  poor  and  jerky  in  character.  The  veins  of  the 
neck  were  a  little  full,  and  there  was  a  slight  amount  of  true 
pulsation  in  them  ;  there  was  also  some  excess  of  arterial  pulsa- 
tion suggestive  of  the  kind  observable  in  Graves's  disease.  There 
w^as  no  dilatation  of  the  heart,  the  apex  being  in  the  nipple  line, 
and  there  was  no  abnormal  cardiac  pulsation.  The  cardiac 
impulse,  though  forcible,  was  not  well  sustained,  and  the  first 
sound  of  the  heart,  though  loud,  was  unduly  short  and  jerky, 
giving  an  impression  of  ineffectiveness.  The  patient  com- 
plained often  of  feeling  her  heart  thumping  in  her  chest,  and  she 
also  had  palpitation  and  breathlessness  on  exertion — such  as 
rumiing,  or  on  hurrying  upstairs.  Palpitation  and  dyspnoea 
on  exertion  were  the  chief  symptoms  of  which  the  patient  com- 
plained, and  it  looked  very  much  as  if  it  were  a  case  of  muscular 
failure  of  the  heart  without  definite  enlargement,  resulting  from 
a  combination  of  nervous  and  physical  overstrain. 

She  was  treated  by  rest  and  tonics  under  thoroughly  con- 
genial surroundings  for  some  weeks,  and  belladonna  was  given 
in  view  of  the  palpitation  and  the  other  symptoms  suggestive  of 
Graves's  disease.  Nevertheless,  after  six  weeks,  she  still  com- 
jjlained  that  any  shght  exertion — such  as  lifting  a  child  into  a 
chair— would  be  apt  to  start  an  attack  of  palpitation  and  breath- 
lessness that  would  last  for  some  hours,  or  any  sudden  call 
upon  the  nervous  system — such  as  seeing  an  unexpected  friend 
or  playing  a  somewhat  difficult  hymn-tune  on  the  piano  before 
the  family  she  was  staying  with — would  have  the  same  effect. 

There  was,  however,  one  symptom  which  was  not  quite  in 
keeping  with  the  above  diagnosis,  and  it  was  not  until  the  symp- 
toms failed  to  yield  to  treatment  that  seemed  eminently 
calculated  to  relieve  them  that  its  importance  was  recognised. 
This  was  the  fact  that  the  palpitation  would  sometimes  come 
on  at  night  or  in  the  afternoon  or  evening  when  no  cause  at  all 
for  it  was  apparent.  Other  facts  also  were  ehcited,  which  if  the 
patient  had  remembered  earlier  on  would  have  helped  to  clear 
up  the  diagnosis.  For  instance,  she  stated  that  riding  in  a 
shaky  motor-bus  always  made  her  feel  bad,  and  that  once  it 
so  upset  her  heart  that  she  nearly  fainted  and  had  to  get  out. 
This  is  a  most  characteristic  symptom  of  irritability  of  the 
transverse  colon,   the  vibration  setting  up  in  it  spasmodic 


PALPITATION  117 

contractions  which  give  rise  either  to  pain  or  simply,  as  in  this 
case,  to  reflex  disturbances  (see  also  case  at  p.  130). 

She  also  stated  that  the  thumping  of  her  heart  was  apt  to 
be  bad  two  hours  after  a  meal. 

In  consideration  of  the  fact  that  circulatory  disturbance 
might  have  been  of  reflex  origin,  and  due  to  abnormal  irrita- 
bility of  the  colon,  the  abdomen  had  several  times  been  carefully 
examined,  and  although  on  one  or  two  occasions  a  slight  amount 
of  colon  irritabihty  was  observable,  it  was  apparently  insufficient 
to  justify  a  diagnosis  of  reflex  cardiac  disturbance.  About  the 
time,  however,  that  the  history  of  nocturnal  attacks  of  palpita- 
tion was  obtained,  the  transverse  and  ascending  colon  was  on 
one  occasion  found  to  be  markedly  hard  and  tender  in  places. 
The  treatment  of  the  case  was  therefore  changed,  and  definitely 
cardiac  remedies  were  replaced  by  fairly  fuU  doses  of  hyos- 
cyamus  with  an  intestinal  antiseptic.  This  treatment  had  an 
almost  immediate  effect  in  the  rehef  of  the  patient's  symptoms, 
and  she  at  one  began  to  improve.  After  only  a  week  or  so  she 
expressed  the  opinion  that  I  had  now  found  the  right  medicine 
for  her. 

While  freely  recognising  the  possibility  of  error  in  ascribing 
any  particular  result  to  any  particular  remedy,  there  was  in 
this  case  abundant  reason  for  coming  to  the  conclusion  that  the 
cardiac  symptoms,  though  pointing  strongly  to  genuine  cardiac 
failure,  were  in  reality  only  of  reflex  origin  and  secondary  to 
abnormal  irritabihty  of  the  colon.  Another  point  in  this  case 
was  the  presence  of  well-marked  colon  irritability  without  the 
presence  of  an  adequate  amount  of  pain,  thus  suggesting  that 
the  afferent  impulses,  which  ought  to  have  given  rise  to  pain  and 
were  not  doing  so,  w^ere  producing  nervous  phenomena  of  some 
other  description. 

Palpitation  as  a  cardiac  habit  persisting  after  the  recovery 
from  myocardial  weakness. — When  dealing  with  the  subject 
of  leg  pains  of  circulatory  origin  a  remarkable  case  is  given 
where  a  disturbance  of  the  cnculation  in  the  legs,  lasting  six 
months,  was  evidently  due  to  the  retention  of  abnormal  action 
on  the  part  of  the  vasomotor  mechanism  as  a  matter  of 
habit. 

The  vasomotor  mechanism  had  got  into  the  habit  of  a 
sluggish  and  incomplete  response  to  the  calls  for  vaso-dilatation 
which  came  fi'om  the  muscles  during  exertion,  and  the  habit 


118 


LATER  LIFE 


was  cured   by  increasing  the  stimulus  to  vaso-dilatation  by 
greater  violence  and  suddenness  of  movement. 

Clinical  experience  shows  that  the  cardiac  mechanism 
also  may  suffer  in  the  same  way,  and  that  after  a  period  of 
extreme  weakness  from  myocardial  disease,  the  palpitation 
and  faintness  which  were  symptomatic  of  the  weakness,  may 
be  retained  by  the  mechanism  as  a  habit  after  the  heart  has 
regained  its  strength.     In  such  a  case  as  this,  reliance  has  to 

Small  Hkakt  in  Myocakdial  Weakness 


Fig.  16. 


Dr.  G.,  aged  twenty-six,  March  24.  Myo- 
cardial weakness  after  dip}itheria.  No  cardiac 
dullness  at  all.  Gastric  resonance  up  to  the 
fourth  rib.  (Absolute  liver  dullness  approxi- 
mate only.) 


Fig.  17. 

Dr.  G.,  April  8.  Heart  now  shows  a  trace 
of  relative  duUness  in  the  fourth  space  and 
a  little  right  ventricle  pulsation.  Still  some 
gastric  resonance  up  to  the  fourth  rib. 


be  placed  on  the  cardiac  phenomena  which  show  return  of 
strength  in  the  heart  wall,  and  the  symptom  must  be  ignored 
from  the  point  of  view  of  diagnosis,  in  spite  of  the  protestations 
of  the  patient. 

To  do  so  requires  considerable  boldness  on  the  part  of 
the  physician,  for  it  is  not  as  a  rule  wise  in  a  case  of  myocardial 
weakness  to  encourage  and  almost  force  the  patient  to  get 
out  of  bed,  in  spite  of  the  fact  that  it  brings  on  troublesome 
palpitation  or  even  a  sense  of  faintness  and  fear  of  impending 
death. 

It  was  only  the  absolute  reliance  of  the  writer  upon  the 


DIAGNOSTIC  DIFFICULTIES 


119 


signs  of  heart  weakness,  which  are  described  in  the  preceding 

pages,  that  gave  him  confidence  in  ignoring  the  symptoms 

of  heart  weakness  in  the  two  cases  which  are  here  recorded, 

because  they  were  in  conflict  with  the  physical  signs  of  returning 

cardiac  strength.    The  first  case  is  the  young  man,  whose  case 

is  shortly  reported  on  p.  182  as  an  instance  of  high  diaphragm 

and  small  heart  in  acute  myocardial  failure  after  influenza. 

When  at  its  worst  the  heart  weakness  was  so  great  that  faint- 

ness  and  even  definite  fainting  attacks  were  caused   by  the 

least  exertion.     The    patient 

was   even   afraid   to   hft   his 

arm  as  he  lay  in  bed  because 

of    the    faintness    which   the 

exertion  produced.   The  heart, 

however,  gi-a dually  recovered 

its    strength,     and     in     the 

course    of    some    weeks    the 

cardiac    dullness   had    nearly 

returned  to  normal.     He  still 

had,  however,  the  same  feeling 

of  faintness,  and  was  afraid 

to  make  any  effort. 

Reljdng,  however,  upon 
the  physical  signs  of  returning 
strength,  he  was  encouraged 
to  make  more  effort ;  but  so 
marked  were    his    symptoms 

that  he  finally  had  to  be  compelled  to  exert  himself,  and 
it  was  only  after  finding  that  his  symptoms  were  not  increased 
by  exertion  that  he  was  willing  to  accept  his  doctor's  advice. 

Another  similar  case  is  that  of  a  lady  (a  doctor)  who  had  a 
severe  attack  of  myocardial  weakness  after  diphtheria.  The 
case  has  already  been  referred  to  at  p.  68  as  a  good  illustration 
of  heart  failure  with  small  heart,  and  is  worth  recording  in 
some  detail  here. 

The  patient  was  a  lady  aged  about  twenty-six,  who  had  had  an 
attack  of  diphtheria  six  weeks  previously.  She  had  no  paralysis; 
but  had  had  heart  attacks  since  her  illness.  She  was  very  weak, 
and  any  exertion  would  bring  on  attacks  of  cardiac  irregularity 


Fig.  18. 

Dr.  Gr.,  June  6.  Heart  stronger ;  cardiac 
dullness  larger;  gastric  resonance  lower;  liver 
dullness  still  very  small. 


120  LATER  LIFE 

and  intermission,  which  made  her  afraid  to  move  at  all.  She 
had  been  confined  to  bed  since  her  attack  of  diphtheria.  The 
pulse  wave  was  of  very  poor  volume  and  weak,  but  the  artery 
was  kept  relatively  full ;  a  weak  pulse  of  relatively  high  tension, 
such  as  is  often  found  in  myocardial  weakness.  On  examining 
the  heart,  no  relative  cardiac  dullness  could  be  detected,  and 
the  gastric  resonance  was  up  to  the  fourth  rib,  giving  the  appear- 
ance shown  in  fig.  16.  The  heart  sounds  were  very  weak  and 
wanting  in  tone,  and  there  was  no  trace  of  cardiac  pulsation. 
The  liver  was  not  carefully  noted  for  fear  of  disturbing  the 
patient.  In  the  figure  it  is  drawn  the  same  as  at  the  next  visit. 
She  was  given  calcium  lactate.  When  seen  a  fortnight  later, 
she  was  better.  There  was  a  trace  of  relative  cardiac  dullness 
and  of  pulsation  in  the  fourth  interspace,  but  the  resonance  of 
the  stomach  could  still  be  detected  up  to  the  lower  border  of 
the  fourth  rib.  The  pulse  was  a  little  fuller  and  the  heart 
sounds  not  quite  so  weak.  I  have  no  note  of  the  veins  of 
the  neck,  but  I  remember  them  as  being  empty  with  much 
hollowing  behind  the  clavicles  (see  fig.  17). 

The  patient  progressed  slowly  but  steadily,  and  by  the 
beginning  of  June  she  was  decidedly  stronger.  The  relative 
cardiac  dullness  now  extended  for  some  2|  or  3  inches  in  the 
fourth  interspace ;  the  apex  was  just  felt  in  the  fifth  space,  and 
there  was  a  trace  of  pulsation  in  the  third  interspace.  The 
heart  sounds  were  much  stronger,  as  was  also  the  pulse,  though 
the  blood  pressure  was  now  only  90  mm.  of  mercury.  The 
liver  had  not  increased  in  size,  though  the  gastric  resonance  now 
only  reached  to  the  fifth  rib  (see  fig.  18). 

After  two  or  three  weeks  more,  the  heart  was  evidently 
stronger,  and  by  the  examination  of  the  chest  I  was  so  sure  of 
this,  that  I  advised  the  patient  to  get  up,  though  she  was  very 
reluctant  to  do  so,  because  such  a  little  exertion  give  her  cardiac 
discomfort.  The  first  few  attempts  at  getting  up  brought  on 
attacks  of  palpitation  and  cardiac  discomfort,  and  made  her 
afraid  to  attempt  to  do  so  any  more.  An  examination  of  the 
heart,  however,  showed  that  even  when  she  felt  ill  it  was  not 
materially  affected,  and  she  was  therefore  advised  to  continue 
getting  up,  but  was  told  that  when  the  attacks  came  on  she 
must  just  rest  till  they  passed  ofi.  She  was  sent  away  to  the 
seaside  before  she  herself  felt  fit,  but  with  no  bad  results,  and 
at  the  end  of  July  reported  having  had  no  heart  attack  for 
several  weeks,  but  that  her  powers  of  walking  about  were  still 
very  limited,  and  she  had  to  use  a  Bath  chair  a  good  deal.     In 


FAINTNESS  121 

this  case  the  irritable  weakness  of  the  heart  remained  as  a 
cardiac  habit  after  the  muscle  had  really  recovered  itself  and  if  in 
this  case  the  medical  adviser  had  been  guided  by  the  patient's 
symptoms  of  cardiac  distress  her  recovery  would  in  all 
probability  have  been  delayed  many  weeks  and  possibly 
even  months, 

Faintness 

The  symptom  of  faintness,  important  as  it  is  in  the  diagnosis 
of  cardiac  failure,  is,  nevertheless,  one  whose  true  value  it  is 
very  difficult  to  appraise  ;  for  there  are  other  causes  of  recurrent 
fainting  attacks,  such  as  might  be  due  to  cardiac  failure.  Of 
these  by  far  the  most  important  is  labjainthine  disturbance, 
and  that  associated  with  high  blood  pressm'e  is  specially  likely 
to  give  rise  to  an  error  in  diagnosis.  The  misleading  points 
in  such  a  case  are  the  suddenness  of  the  attack,  which  may 
come  on  without  any  warning,  and  consists  in  a  simple  faint 
without  any  vertigo ;  it  is,  moreover,  usually  followed  by  a  sense 
of  extreme  weakness  and  prostration,  and  the  patients  will 
often  not  believe  that  the  wealaiess  is  of  nervous  and  not  of 
cardiac  origin.  The  points  in  favom-  of  the  case  really  belong- 
ing to  what  is  commonly  called  Meniere's  disease  are  these  : 
(1)  sudden  rotation  of  the  patient  will  in  such  a  case  be  very 
likely  to  demonstrate  the  presence  of  vertigo,  and  thus  help 
to  clear  up  the  case  ;  (2)  the  occurrence  of  vomiting  or  nausea 
with  the  fainting  attack  is  very  suggestive  of  its  cerebral 
origin,  although  vomiting  may  accompany  an  ordinary  cardiac 
fainting  attack  ;  (3)  the  presence  of  vertigo  after  the  attack 
is  often  a  valuable  aid  to  the  formation  of  a  correct  diagnosis. 
In  addition  to  these  positive  symptoms,  the  endeavour  must 
be  made  to  exclude  true  cardiac  weakness,  and  in  this  con- 
nection the  old  proverb  comes  to  our  aid  :  '  The  strength  of  a 
chain  is  that  of  its  weakest  link.'  If  the  patient  can  ever 
walk  upstairs  easily  without  breathlessness,  or  walk  up  hills 
at  a  good  pace,  the  faintness  is  not  of  organic  cardiac  origin, 
and  there  need  be  no  fear  as  to  the  presence  of  fatty  or 
other  degeneration  of  the  heart.  Here  is  a  striking  case 
where  an  error  of  diagnosis  deprived  a  man  of  many  years 
of  usefulness. 


122  LATER  LIFE 

The  patient  was  a  gentleman  aged  sixty-nine  who  had 
suffered  from  severe  attacks  of  faintness  and  giddiness  for  four 
five  or  years  or  more.  They  were  not  very  frequent — some- 
times once  a  week — and  sometimes  he  would  go  for  months 
without  one. 

He  saw  a  consultant  who  had  a  well-earned  reputation  in 
connection  with  cardiac  diagnosis  and  treatment,  and  was 
told  that  his  attacks  were  mainly  of  cardiac  origin,  and  I  believe 
also  there  was  some  suggestion  that  disease  of  the  vertebral 
arteries,  by  further  interfering  with  the  blood  supply  to  the 
brain,  had  something  to  do  with  the  severity  of  his  fainting 
attacks. 

He  was  told  that  any  one  of  these  attacks  might  prove  fatal ; 
was  told  to  give  up  all  his  public  work,  in  which  he  was  much 
interested,  and  live  the  life  of  an  invalid  ;  and  for  three  or  four 
years  he  lived  in  the  constant  expectation  of  sudden  death  (I 
will  not  say  fear  of  death,  for  he  did  not  fear  it).  His  wife,  too, 
was  prepared  to  have  him  brought  back  to  the  house  dead  every 
time  he  left  it.  A  truly  tragic  and  painful  experience.  Some 
five  years  or  so  after  the  original  diagnosis  was  made,  he  came 
to  me,  and  I  was  surprised  to  find  that  in  many  respects  his 
attacks  were  typical  of  Meniere's  disease,  and  not  of  fainting  of 
cardiac  origin ;  moreover,  on  questioning  the  patient,  I  could 
find  no  evidence  of  there  ever  having  been  marked  dyspnoea 
or  exhaustion  on  ordinary  exertion  even  when  the  attacks  were 
at  their  worst,  nor  were  they  definitely  brought  on  by  exertion, 
so  far  as  I  could  ascertain.  There  was,  moreover,  a  considerable 
degree  of  deafness  in  the  ear,  and  the  Eustachian  tube  on  that 
side  was  quite  obstructed  and  no  air  could  be  got  in  with  the 
Eustachian  catheter.  As  I  had  the  catheter  in  place,  I  passed 
a  bougie  into  the  tympanum,  and  this  single  opening  up  of  the 
tube  seemed  to  suffice  to  relieve  him.  At  the  time  of  his  visit 
to  me,  he  was  only  having  attacks  every  few  months,  and  after 
his  visit  to  me  I  believe  he  did  not  have  another  attack. 

I  of  course  told  him  my  view  of  his  case,  and  he  at  once 
resumed  the  degi'ee  of  activity  which  his  age  rendered  advis- 
able, and  without  any  unsatisfactory  results. 

Here  is  another  case  somewhat  similar.  Mrs.  D.,  aged  sixty- 
one,  a  well-nourished  woman  of  fairly  healthy  appearance  and 
with  no  definite  signs  of  cardiac  failure,  complained  that  two 
years  ago  she  had  a  bad  fainting  attack  on  first  getting  out  of  bed 


FAINTNESS  123 

in  the  morning.  A  month  or  two  later,  she  had  another,  falUng 
unconscious  on  the  floor  of  her  sitting-room  as  she  was  about 
to  go  out  of  the  house.  The  attacks  since  then  have  occurred 
every  few  months — sometimes  the  interval  will  be  one  month, 
sometimes  three  ;  but  until  August  1912,  when  she  had  two  in 
one  week,  the  interval  had  never  been  less  than  a  month.  From 
January  to  March  1913,  she  only  had  three  attacks.  She  was 
afraid  to  go  out  into  the  street  for  fear  of  one  coming  on  ;  but  so 
far  this  had  not  happened,  the  attacks  mostly  being  in  bed  or 
early  in  the  morning.  This  history  of  course  pointed  clearly  to 
the  attacks  being  either  niild  epilepsy  or  of  labyrinthine  origin. 

That  they  were  not  cardiac  was  shown  by  the  fact  that 
exertion  never  caused  them  ;  that  the  patient,  though  rather 
breathless  on  walking  uphill,  did  not  suffer  at  all  from  serious 
dyspnoea,  and  could  go  upstairs  fairly  easily.  She  was  con- 
vinced that  her  heart  was  at  fault.  '  Her  circulation  was  bad.' 
The  fingers  were  very  apt  to  go  dead  in  cold  weather,  and  she  at 
times  felt  weak  and  ill.  The  heart  certainly  was  not  strong,  but 
it  was  not  weak  enough  to  justify  a  diagnosis  of  the  fainting 
attacks  being  due  to  myocardial  weakness.  The  cardiac  area 
was  only  a  little  smaller  than  normal  ;  the  sounds  only  a  little 
weak,  but  the  jugular  bulb  pulsation  was  of  fair  strength.  The 
gastric  resonance  was  a  little  high — i.e.,  to  the  upper  border  of 
the  sixth  rib — and  the  absolute  dullness  of  the  liver  a  little 
diminished  in  size.  The  blood  pressure  was  170.  The  daily 
excretion  of  purin  bases  was  0*46  instead  of  being  under  0*2 
as  it  should  be,  and  there  were  580  grains  of  urea  secreted  in 
the  twenty-four  hours. 

On  testing  the  semicircular  canals  there  was  distinct  hyper- 
8BSthesia  to  rotation  in  the  positive  direction,  the  after-sensation 
lasting  much  longer  than  the  original  rotation  ;  while  for  nega- 
tive rotation  the  after-sensation  was  about  normal.  Although 
she  was  only  rotated  slowly  (three  seconds  or  so  being  taken 
for  a  rotation  through  three-quarters  of  a  circle),  and  the  test 
was  only  once  repeated,  there  was  a  little  unsteadiness  in  the 
carriage  of  the  head  afterwards  and  the  patient  complained  of 
feeling  very  '  giddy  and  horrid,'  and  afterwards  she  said  she  felt 
confused  and  hardly  able  to  hold  her  head  up. 

In  addition  to  the  high  blood  pressure  and  abnormal  intake 
of  purins  there  was  also  a  considerable  amount  of  colon  tender- 
ness and  irritability,  and  quite  enough  to  be  a  possible  cause  of 
considerable  reflex  cardiac  or  circulatory  disturbance. 

A  confident  diagnosis  was  given  in  this  case  that  the  patient 


124  LATER  LIFE 

need  not  fear  as  to  her  heart.  In  a  case  like  this  it  is  probable 
that  local  treatment  directed  to  the  opening  of  the  Eustachian 
tubes  would  be  necessary  as  well  as  that  directed  to  the  lowering 
of  the  blood  pressure  by  lessening  the  abundance  of  the  waste 
products  of  metabolism  in  the  circulation. 

Another  well-known  cause  of  attacks  of  faintness  is  reflex 
gastric  disturbance,  although  actual  fainting  is  far  less  common 
from  this  cause  than  a  sense  of  faintness  often  accompanied 
by  a  little  vertigo,  such  as  often  precedes  an  ordinary  fainting 
attack. 

I  have  just  given  two  cases  where  cardiac  failure  was 
simulated  by  fainting  due  to  some  other  cause.  I  will  now 
speak  of  a  case  where  faintness  of  cardiac  origin  was  diagnosed 
and  treated  as  being  simply  of  reflex  gastric  origin. 

Although  I  did  not  personally  examine  the  patient,  the 
circumstances  were  known  to  me,  and  I  give  a  probable 
analysis  of  the  case  to  illustrate  how  the  principles,  here  laid 
down,  would  apply  where — as  in  this  instance — there  was 
myocardial  degeneration  that  could  easily  be  overlooked. 

The  patient  was  an  elderly  gentleman  of  thoroughly  healthy 
appearance  and  active  in  mind  and  body,  and  almost  the  only 
thing  he  complained  of  was  a  slight  passing  feeling  of  faintness 
or  giddiness  that,  while  rather  alarming  his  friends,  did  not  cause 
him  any  serious  inconvenience.  He  was  noticed  to  be  decidedly 
breathless  when  walking  too  fast,  especially  uphill ;  but  as  it 
had  only  gradually  increased  in  degree,  and  did  not  trouble  him 
in  ordinary  exertion  he  did  not  think  anything  of  it.  The 
seriousness  of  his  condition  was  not  recognised  till,  while  ap- 
parently in  perfect  health,  he  one  day  suddenly  had  a  fainting 
attack  while  standing,  during  the  act  of  micturition,  and  never 
recovered  consciousness. 

He  had  seen  a  consultant  as  to  his  attacks  of  faintness,  and 
he  had  treated  them  as  being  simply  gastric  in  origin. 

What  were  the  physical  signs  which  might  have  revealed 
the  presence  of  myocardial  degeneration  ?  From  my  ex- 
perience of  this  type  of  cardiac  failure,  I  think  I  shall  not  be 
far  wrong  in  suggesting  that  if  the  case  had  been  studied  in 
the  manner  here  suggested  the  following  important  facts 
would  have  been  brought  out. 


DIAGNOSTIC  DIFFICULTIES  125 

First  as  to  the  cardiac  action.  The  pulse  was  probably  a 
good  normal  pulse  for  a  man  of  his  age,  but  probably  careful 
observation  would  have  sho\\Ti  that  it  collapsed  a  little  too 
readily  between  the  beats,  giving  it  rather  a  short  jerky  type. 
Had  it  been  poor  and  weak,  the  able  speciahst  he  went  to  see 
would  certainly  have  recognised  myocardial  degeneration  as 
the  cause  of  his  faintness.  As  regards  the  impulse  of  the  left 
ventricle,  the  apex  beat  may  or  may  not  have  been  palpable. 
The  probability  is  that  there  was  no  cardiac  impulse  at  all. 

As  regards  the  right  ventricle.  The  veins  of  the  neck 
would  have  been  empty  and  the  supra-clavicular  fossse  deep. 
The  jugular  bulb  would  almost  certainly  have  been  quite 
indistinguishable  owing  to  emptiness  of  the  vein  and  absence 
of  pulsation  ;  or,  if  after  exertion  the  veins  of  the  neck  filled  up, 
as  they  might  do  then,  there  would  be  practically  no  pulsation 
in  them  except  a  slight  amount  of  false  pulsation.  There 
would  be  no  pulsation  to  left  of  the  sternum  or  in  the  epigas- 
trium, showing  weakness  and  emptiness  of  the  right  side  of 
the  heart.  In  addition  to  these  there  would  be  weU-marked 
signs  that  the  amount  of  blood  in  active  circulation  was  less 
than  normal — namely,  the  gastric  resonance  would  be  up 
above  the  normal  level,  and  quite  possibly  well  into  the 
fifth  interspace,  and  the  dullness  of  the  liver  and  the  heart 
would  probably  be  less  than  normal. 

This  is  a  pictm'e  of  what  such  a  case  might  well  show; 
but  be  it  noted  there  is  not  a  single  one  of  these  signs  that 
might  not  be  passed  over  as  being  quite  unimportant,  even  if  it 
w^ere  observed  at  all  ;  and  not  one  of  them,  except  the  absence 
of  pulsation  in  the  jugular  bulb,  that  ought  not  rightly  to  be 
passed  over  as  probably  being  quite  unimportant  if  it  occurred 
singly  ;  but  the  occurrence  of  aU  the  signs  together,  insignificant 
though  they  may  be,  makes  a  certain  and  unmistakable  pictm-e 
of  dangerous  myocardial  degeneration — probably  fatty  and 
due  to  disease  of  the  coronary  artery  supplying  the  right 
ventricle  and  to  a  less  extent  the  left. 

The  difficulty  of  this  case  lay  undoubtedly  in  the  fact 
that  the  right  ventricle  was  in  the  main  affected,  while  the 
left  was  fahdy  strong  and  weU  nourished. 

His  activity  of  mind  and  body  depended  on  this  fact — that 


126  LATER  LIFE 

the  left  ventricle  was  capable  of  any  ordinary  call  that  he  made 
upon  it  e^'-^n  in  the  matter  of  public  speaking  and  much 
travelling  about.  The  weakness  of  the  right  side  showed  itself 
in  the  very  marked  dyspnoea  that  accompanied  any  over- 
stepping of  the  limits  of  what  the  right  ventricle  was  able  to 
accomplish. 

In  such  a  case  as  this  the  total  amount  of  blood  in  circu- 
lation would  be  cut  down  by  the  inability  of  the  right  ventricle 
to  pass  the  normal  amount  through  the  lungs,  and  nature's 
compensatory  mechanism  would  cut  down  the  blood  in  active 
circulation  to  this  amount.  In  such  a  case  as  this  it  is  some- 
times noticeable  that  distinct  dyspnoea  is  produced  while 
taking  the  blood  pressure  as  soon  as  the  pressure  on  the  veins 
of  the  arm  is  great  enough  to  interfere  with  the  supply  of 
blood  to  the  heart  (see  p.  140).  The  occurrence  of  such  dyspncjea 
in  this  case  would  have  given  confirmatory  evidence  as  to 
myocardial  degeneration. 

The  fatal  fainting  attack  took  place,  in  aU  probability, 
because  the  sudden  emptying  of  the  bladder  lessened  the 
return  of  blood  to  the  heart  by  delaying  its  return  from  the 
abdominal  veins,  in  the  manner  pointed  out  many  years  ago 
by  Sir  Lauder  Brunton. 

Had  the  diagnosis  of  myocardial  weakness  been  made,  some 
years  might  have  been  added  to  this  patient's  hfe ;  for  in  all 
such  cases  the  caution  should  be  given  never  to  pass  water 
when  standing  up,  but  only  when  sitting  or  squatting.  It 
is  an  interesting  fact  that  the  natives  of  India  always  urinate 
in  this  latter  attitude ;  and  it  is  possible  that  the  occm-rence, 
not  infrequently,  of  sudden  deaths  while  micturating  standing, 
did,  centuries  ago,  give  rise  to  the  superstitious  belief  that 
to  do  so  was  offensive  to  the  Euler  of  the  Umverse,  and  hence 
led  to  the  adoption  of  a  more  humble  attitude. 


Anginal  Pain 

There  are  diagnostic  difficulties  associated  with  the 
occurrence  of  anginal  pain ;  but  these  are  mainly  as  regards 
the  differentiation  between  the  pain  arising  from  a  temporary 
spasm  of  the  arteries  due  to  reflex  disturbance— the  so-called 


ANGINAL  PAIN  127 

'  vasomotor  angina,'  and  that  duo  to  organic  disease  of 
the  heart  or  the  arteries.  There  is  Httle  if  any  ?'isk  here  of 
mistaking  a  true  cardiac  pain  for  one  merely  of  gastric  origin. 

As  to  the  diagnosis  of  angina  from  other  forms  of  pain  Httle 
need  be  said  here,  as  the  subject  is  fully  dealt  with  in  the  many 
books  on  the  heart  which  exist. 

The  diagnosis  of  true  angina  rests  upon  similar  observations 
to  those  already  referred  to — namely,  especially  upon  observing 
the  strength  of  the  heart  as  judged  by  physical  examination 
and  by  noting  the  amount  of  exertion  the  patient  can  take 
without  bringing  on  an  attack  of  pain. 

When  noting  the  strength  of  the  heart  it  must  not  be  for- 
gotten that  true  angina  pectoris  can  occur  in  a  patient  with  a 
strong  heart,  when  the  work  it  has  to  do  is  sufficiently  increased 
by  high  arterial  resistance  and  loss  of  elasticity  of  the  first  part 
of  the  aorta,  just  as  readily  as  it  can  occur  in  a  heart  with 
weakened  muscle,  which  is  striving  to  carry  on  the  circulation 
under  normal  arterial  conditions. 

In  illustration  of  this  subject  it  may  be  of  interest  to  give 
two  striking  cases  of  reflex  angina,  and  in  both  the  cause  was  the 
irritability  of  the  colon,  which  results  in  the  condition  which  I 
have  called  '  colon  dyspepsia,'  and  which  would  be  less  correctly 
embraced  under  the  well-known  term,  mucous  colitis. 

The  following  is  a  case  of  what  might  be  called  vasomotor 
angina,  which  might  very  easily  be  mistaken  for  true  angina,  due 
to  cardiac  failm-e.  The  patient  was  a  lady  aged  forty-two,  who 
for  some  years  had  had  occasional  attacks  of  pain  in  the  chest, 
usually  brought  on  by  exertion.  The  pain  was  usually  located 
just  over  the  heart  at  about  the  level  of  the  fifth  and  sixth  ribs. 
Sometimes  it  would  be  felt  to  run  up  the  left  side  of  the  neck  as 
far  as  the  angle  of  the  jaw,  and  for  five  minutes  or  so  it  would  be 
like  a  severe  neuralgia.  In  the  more  severe  attacks  it  started 
in  the  left  sub-clavicular  region  about  the  coracoid  process,  and 
would  run  up  over  the  shoulder  and  right  down  the  arm  to 
the  thumb,  the  pain  being  mainly  along  a  narrow  area  an  inch 
or  so  wide,  running  down  the  front  of  the  upper  arm  and  the 
radial  border  of  the  forearm  to  the  thumb.  The  pain  was  very 
severe  under  the  thumbnail.  In  a  very  severe  attack  the  only 
other  place  where  she  felt  pain  was  under  the  nail  of  the  left 
great  toe.     The  pain  was  often  so  severe  here  as  to  be  almost 


128  LATER  LIFE 

unbearable.  The  toe,  too,  was  often  so  tender  of  an  evening 
that  she  could  not  even  wear  soft  felt  slippers.  The  pain  was 
usually  accompanied  by  a  sense  of  suffocation  which  she  de- 
scribes as  '  a  terrible  gasping  sensation,  which  made  her  feel  as 
if  she  were  dying.'  She  often  also  had  palpitation  with  the 
attacks.  When  the  attacks  were  severe,  the  feeling  that  death 
was  impending  was  very  strong,  and  sometimes  for  many  even- 
ings in  succession  she  would  sit  up  till  quite  late  at  night  because 
she  was  afraid  to  go  to  sleep,  owing  to  the  uncertainty  she  felt 
as  to  whether  she  would  be  alive  in  the  morning. 

It  seemed  quite  certain  that  these  attacks  were  associated 
with  cardiac  weakness ;  for  hurrying  upstairs  would  always 
bring  on  pain,  and  anything  lowering  the  nerve  tone  would 
have  the  same  effect.  During  the  four  months  prior  to  my 
seeing  her,  she  had  had  much  domestic  anxiety  and  physical 
strain  and  bereavement,  in  that  she  personally  nursed  a  child 
and  her  husband,  both  of  whom  died  within  a  month  or  two  of 
each  other.  The  strain  of  this  time  had  greatly  increased  the 
frequency  of  the  attacks  of  pain,  and  latterly  they  had  been  as 
frequent  as  four  and  five  times  a  day. 

Their  cardiac  nature  was  also  suggested  by  the  fact  that 
nitroglycerine  would  relieve  them  in  ten  or  fifteen  minutes,  and 
that  if  nothing  was  taken  they  would  last  some  hours. 

Another  point  was  that  when  the  sense  of  suffocation  was 
severe  she  could  sometimes  by  a  single  '  long  breath  '  get  rehef 
for  five  minutes.  More  often,  and  especially  of  late,  she  cannot 
do  this,  and  '  the  breath  seems  to  stop  half-way.' 

A  point  in  the  history  which  is  not  quite  characteristic  of 
pure  cardiac  angina  is  the  fact  that  she  was  very  apt  to  have  an 
attack  on  going  to  bed  at  night,  lasting  a  quarter  of  an  hour  or 
so.  These  were  often  associated  with  severe  abdominal  pain 
and  a  sense  of  a  band  of  iron  right  across  the  abdomen  just  at  or 
above  the  umbilicus. 

She  also  had  occasionally  severe  attacks  of  prostration 
associated  with  symptoms  of  Eeynaud's  disease. 

This  is  an  account  of  a  typical  one. 

One  Saturday  last  summer  a  gastric  attack  began  just  before 
she  started  on  a  journey  to  London.  It  began  with  an  intense 
distaste  for  food  and  she  could  not  even  drink  water. 

Nevertheless,  she  persevered  with  her  journey,  spent  the 
whole  of  Sunday  in  bed,  and  got  back  to  Birmingham  at 
4.40  P.M.  Monday.  During  the  whole  of  that  time  she  asserts 
that  she  touched  neither  food  nor  water.     She  says  also  that 


ANGINAL  PAIN  129 

the  hands  and  feet  were  blue-grey  and  dead  from  9  a.m.  on  the 
Sunday  till  the  Monday  evening.  She  also  had  a  very  severe 
headache.  The  blueness  of  the  hands  is  a  feature  of  every 
severe  attack. 

On  examining  her,  the  heart  was  found  to  be  apparently 
normal  in  size  and  action,  except  that  the  right  ventricular 
sounds  were  a  trifle  louder  than  normal.  The  venous  circulation, 
too,  was  normal,  and  there  was  nothing  to  suggest  myocardial 
failure.  On  examining  the  abdomen  it  was  found  that  the  caecum 
was  markedly  hard  and  tender,  as  was  also  the  sigmoid  flexure  ; 
but  the  somewhat  severe  pain  which  moderately  firm  palpation 
of  the  caecum  caused  had  a  most  interesting  result.  It 
immediately  produced  a  most  marked  flushing  of  the  face  and 
a  httle  blueness  of  the  hands,  accompanied  by  one  of  her  typical 
attacks  of  anginal  pain  in  the  heart  and  down  the  left  arm. 
•  In  connection  with  this  tenderness  of  the  caecum,  and  the  fact 
that  pain  there  could  produce  an  attack  of  angina,  she  said  that 
the  right  side  was  always  tender  when  she  had  an  attack,  and 
that  the  attack  seemed  to  start  there  and  then  go  to  her  heart. 

At  a  subsequent  visit  the  transverse  colon  was  found  to  be 
in  a  state  of  extreme  expansile  tone  throughout  its  entire 
length,  and  was  quite  visible  right  across  the  abdomen.  It  was 
expanded  to  about  the  diameter  of  a  lady's  wrist,  and  was  quite 
hard  to  the  touch  and  extremely  tender.  It  was  this  hardening 
up  of  the  transverse  colon  that  gave  the  patient  the  sensation 
she  described  as  severe  pain  accompanied  by  the  feehng  of 
having  an  iron  band  across  the  abdomen.  This,  then,  was  a 
case  of  extremely  irritable  colon.  It  might  well  be  called  colon 
dyspepsia,  for  the  term  mucous  cohtis  was  hardly  appHcable 
— there  being  no  excess  of  mucus  in  the  stools. 

This  patient's  condition  was  very  greatly  improved  by  the 
adequate  treatment  of  her  colon. 

It  was  not  a  case  where  the  pain  showed  the  presence  of 
cardiac  weakness.  The  case  was  one  where  the  powerful 
afferent  impulses  from  the  extremely  irritable  colon — which 
ought  to  have  caused  very  severe  abdominal  pain  (but  did 
not) — expended  all  their  energy  upon  the  vasomotor  mechanism. 
On  reaching  the  cord  through  the  sympathetic  nerves  from  the 
colon,  instead  of  getting  into  the  sensory  tracts  and  causing 
pain,  they,  as  it  were,  lost  their  way  and  got  into  the  vaso- 
motor tracts,  with  the  result  that  they  caused  so  severe  an 

K 


130  LATER  LIFE 

arterial  spasm  that  the  heart  was  overtaxed  and  cardiac  pain 
resulted.  The  deadness  and  blueness  of  the  hands  which 
accompanied  the  pain  was  another  evidence  of  the  arterial 
spasm.  The  severity  of  the  vasomotor  distm'bance  is  shown 
by  such  attacks  as  the  one  recorded  when  the  whole  of  both 
hands  and  feet  remained  dead  and  grey  for  twenty-four  hours. 

The  part  played  in  this  case  by  the  reflex  mechanism  is 
shown  by  the  fact  that  any  circumstances  which  were  calculated 
to  heighten  the  excitabihty  of  that  mechanism  were  sure  to 
increase  the  frequency  and  the  severity  of  her  attacks  of  pain. 

Another  case  of  extreme  interest  is  the  following  : — 

The  patient  was  a  gentleman  of  fifty-five,  whose  pleasm'e,  as 
well  as  the  support  of  his  household,  was  more  or  less  closely 
associated  with  the  following  of  the  hounds  in  the  hunting- 
field. 

He  was  sent  to  me  by  his  doctor  because  of  the  somewhat 
frequent  recurrence,  of  late,  of  severe  pain  in  his  chest,  accom- 
panied by  a  sense  of  weight  and  tightness  across  the  chest,  but 
not  by  breathlessness  or  a  sense  of  impending  death  as  in  the 
last  case.  Another  point  of  some  importance  was  that  nerve 
worry  and  strain  was  far  more  likely  to  bring  on  the  pain  that 
physical  exertion.  When  the  pain  was  liable  to  occur  it  would 
often  come  on,  when  hunting,  with  the  first  gallop  of  the  day, 
and  his  custom  was  to  get  off,  take  a  dose  of  nitroglycerine  till 
the  pain  subsided,  and  then  get  on  again  and  continue  hunting, 
which  he  found  he  could  do  even  throughout  the  whole  day, 
and  on  a  pulling  horse,  without  any  return  of  the  pain.  If 
he  did  not  take  the  nitroglycerine,  the  pain  would  go  off, 
though  less  quickly,  but  would  be  apt  to  recm-,  after  remounting, 
the  next  time  he  had  a  gaUop.  Another  instance  of  the  mode 
of  occurrence  and  disappearance  of  the  pain  is  interesting  and 
instructive.  It  came  on  one  day  when  he  was  walking  to  the 
post,  but  as  he  had  to  catch  it  he — to  use  his  own  expression — 
'  braced  his  shoulders  back  and  clenched  his  arms,'  and  by  the 
time  he  got  to  the  post  the  pain  had  gone. 

The  examination  of  the  heart  suggested  a  certain  amount 
of  cardiac  weakness,  in  that  the  cardiac  area  was  small  and  the 
gastric  resonance  a  little  high  and  the  beat  of  the  heart  and  its 
sounds  rather  feeble.  The  blood  pressure  was  120  mm.,  and  the 
volume  of  the  pulse  very  good.  The  venous  pulsation,  too, 
was  good  in  tone.    No  signs  of  definite  cardiac  weakness  on 


ANGINAL  PAIN 


131 


exertion  could  be  detected.  For  instance,  going  uphill  to 
church  on  a  Sunday  would  bring  on  the  pain,  but  chmbing  hills 
when  on  a  holiday  would  not  (see  fig,  19). 

The  strength  of  a  chain  being  its  weakest  link,  it  was 
evident  that  the  anginal  attacks  could  not  primarily  be  due 
to  cardiac  weakness  or  they  would  always  come  on  when  the 
heart  was  taxed  beyond  a  certain  point.  An  interesting  point 
about  the  case  was  that  on  first  starting  out,  galloping  on  horse- 
back was  almost  certain  to  bring  on  an  attack,  whereas  later 
in  the  day  it  did  not.  Also 
the  attacks  of  pain  often 
came  on  suddenly  and  with- 
out cause,  especially  at  night. 
Both  these  last  two  facts 
point  to  the  possibiHty  of 
the  attacks  arising  reflexly 
from  irritabihty  of  the  colon, 
and  especially  the  transverse 
colon,  to  judge  from  the  fact 
that  shaking  dm^ing  the  act 
of  galloping  was  apt  to  bring 
it  on.  The  fact  that  the  first 
gallop  of  the  day  brought  it  on, 
whereas,  later  on,  galloping 
did  not,  is  quite  characteristic 
of  this  mode  of  onset.  The 
shaking  of  the  transverse 
colon  caused  a  muscular 
spasm  at  first ;   but,  later  on, 

when  the  bowel  got  used  to  the  movement,  no  spasm 
resulted.  The  cessation  of  pain  in  the  bowel  (or  of  reflex 
disturbance  occurring  in  place  of  pain),  in  spite  of  a  continuance 
of  the  movement  that  first  caused  it,  is  a  common  phenomenon 
in  cases  where  the  transverse  colon  is  ii-ritable.  In  this  case  the 
examination  of  the  abdomen  showed  marked  tenderness  of  the 
colon,  and,  fm-ther,  a  history  of  occasional  pain  in  the  gi-oin  was 
obtained.  Moreover,  the  man  was  almost  cured  of  his  cardiac 
symptoms  by  intestinal  antiseptics  and  a  diet  adapted  to  his 
colon  dyspepsia. 

Another  interesting  point  was  this.  Intentional  rough 
handling  of  the  tender  caecum  or  sigmoid  flexure  not  only 
caused  some  of  the'^pain  in  the  chest  fiom  which  he  was  apt  to 

k2 


Fig.  19. 

Colonel  F.,  aged  fifty-five,  January  1911. 
Vasomotor  angina.  Cardiac  area  rather  small, 
and  gastric  resonance  high. 


132  LATER  LIFE 

suffer  as  well  as  pain  in  the  abdomen,  but  it  also  caused  some 
blanching  of  the  fingers  and  hands  (a  tendency  to  '  deadness  '), 
thus  showing  that  definite  arterial  spasm  could  be  produced 
at  will  by  irritation  of  his  colon,  and  giving  strong  evidence 
in  favour  of  his  attacks  being  due  to  a  vasomotor  disturbance, 
whose  source  of  origin  was  the  irritable  colon.  The  diagnosis 
of  such  a  case  as  this  is  not  difficult  if  the  evidence  be  properly 
weighed,  as  was  done  by  his  doctor  who  sent  him  to  me,  as  a 
case  of  false  and  not  true  angina. 

Other  cases  of  false  angina  might  be  given,  but  these  must 
suffice. 

Where  there  is  severe  pain  in  the  upper  part  of  the  abdomen 
it  is  sometimes  not  easy  at  first  to  say  whether  it  be  of 
abdominal  or  cardiac  origin. 

The  Diagnostic  Value  of  Venous  Phenomena 

In  middle  and  later  life  the  venous  phenomena  which  are 
due  to  the  presence  of  tricuspid  regurgitation,  or  which 
characterise  its  absence  when  it  might  reasonably  be  expected 
to  be  present,  are  of  very  great  clinical  importance. 

Although  the  study  of  the  veins  is  of  importance  in  the 
moderately  distensible  heart  of  adult  life,  the  information 
they  give  is  of  greater  value  where  the  heart  is  too  rigid  to 
admit  of  dilatation,  and  the  condition  of  the  veins  is  of  yet 
greater  value  in  cases  where  the  muscular  failure  of  the  heart 
is  so  considerable  that  it  is  unable  to  maintain  a  condition 
of  venous  plethora  at  all. 

In  the  present  connection  the  phenomena  of  venous  plethora 
only  will  first  be  noted. 

The  various  points  from  which  important  information  can 
be  gained  will  now  be  summarised. 

1.  When  first  observing  the  condition  of  the  veins  of  the 
neck  a  distinction  must  be  made  between  the  condition  of  the 
great  veins  (the  innominates  and  the  subclavians)  and  that 
of  the  jugular  and  other  neck  veins  which  are  on  the  distal 
side  of  the  valves  which  guard  the  veins  opening  into  the 
subclavians  and  the  innominates.  There  is  an  important 
reason   for   this    distinction,    because   the   great   veins   form 


VENOUS  PHENOMENA  133 

practically  a  part  of  the  auricular  reservoir  for  supplying  the 
right  ventricle,  and  the  subclavian  valves  may  therefore  be 
regarded  as  cardiac  valves — so  important  is  their  action  in 
the  circulation  of  the  blood.  These  great  veins,  and  the  auricle 
constitute  what  is  practically  the  compensation  reservoir  of 
supply  for  the  right  ventricle,  and  the  blood  in  it  is  always 
kept  under  pressure  by  the  tonic  contraction  of  the  muscles 
in  the  walls  of  the  veins  and  of  the  auricle.  There  is  no  evidence 
of  any  true  relaxation  of  the  walls  of  the  auricle  during  its 
diastole,  and  the  same  is  true  of  the  right  ventricle.  During 
the  phase  of  the  diastole,  which  I  have  called  the  '  relaxation 
phase,'  there  is  still  tonic  activity  on  the  part  of  the  cardiac 
muscle,  and  the  term  relaxation  is  only  a  relative  one.  In 
this  the  cardiac  muscle  is  like  other  muscles  of  the  body  which 
have  their  periods  of  activity  and  of  quiescence,  but  during 
their  quiescence  still  retain  a  certain  measure  of  tonic,  as 
distinct  from  true  contractile,  activity.  This  point  is  well 
brought  out,  and  in  my  opinion  definitely  proved  by  the  careful 
study  of  the  venous  and  cardiac  tracings  which  form  the 
subject  of  Essay  XVII,  p.  489.  This  case  shows  that  the 
blood  in  the  reservoir  is  under  pressure  and  that  waves  can  be 
reflected  backwards  and  forwards  between  the  subclavian 
valves  and  the  wall  of  the  right  ventricle  during  its  relaxation 
period  in  a  manner  that  would  not  be  possible  were  the  walls 
of  the  veins  or  the  ventricle  really  lax  in  any  absolute  sense. 
Fortunately,  natm-e  has  arranged  that  in  one  spot  this  venous 
reservoir  comes  within  om"  reach  for  purposes  of  observation — 
namely,  at  the  spot  where  the  external  jugular  vein  enters 
the  subclavian.  The  valves  which  guard  this  vein  are  situated 
some  little  distance  from  the  subclavian,  and  just  come  within 
reach  of  the  finger  if  pressed  down  behind  the  clavicle.  In 
this  way  we  can  by  palpation  measm-e  the  height  of  the  blood 
pressm-e  in  the  auriculo-venous  reservoir  and  thus  gain  very 
important  information  as  to  the  power  which  is  being  developed 
by  the  right  ventricle,  for  its  beat  can  be  plainly  felt  and  we 
can  also  judge  by  the  feel  of  the  vein  under  the  finger  as  to 
the  presence  or  absence  of  over-distension  and  of  the  strong  beat 
due  to  true  tricuspid  regurgitation.  This  portion  of  the  jugular 
vein  has  been  christened  by  Sir    J.  Mackenzie    '  the  jugular 


134  LATER  LIFE 

bulb,'  in  consequence  of  the  sensation  which  it  gives  to  the 
finger  when  the  pressure  in  the  auriculo-venous  reservoir  is 
raised  above  the  normal,  and  it  seems  a  very  apposite  term. 

The  examination  of  the  jugular  bulb  is  as  important  in 
judging  of  the  work  of  the  right  ventricle  as  the  examination 
of  the  radial  pulse  is  in  the  case  of  the  left  ventricle  ;  and  the 
information  which  it  gives,  as  to  the  power  of  the  cardiac 
muscle,  is,  in  later  life,  even  more  reliable  than  that  given 
by  the  radial  artery.  It  would  be  quite  suitable  to  describe 
the  pulsation  felt  in  the  jugular  bulb  as  ike  venous  pulse. 

In  addition  to  the  information  given  by  the  palpable  impulse 
felt  in  the  jugular  bulb,  it  is  also  possible  to  gain  some  knowledge 
as  to  the  extent  to  which  the  auriculo-venous  reservoir  is  filled 
with  blood,  for  when  the  superior  cava  and  its  branches  are  more 
distended  than  normal  the  hollows  above  the  clavicles  and  in  the 
episternal  notch  are  less  evident  than  when  the  veins  are 
emptier.  When  the  veins  are  much  over-distended  as  a  result 
of  tricuspid  regurgitation  the  pulsation  of  the  subclavians 
or  innominates  may  be  distinctly  visible  and  palpable  behind 
the  clavicles  or  in  the  episternal  notch.  When  the  veins  are 
emptier  than  normal  (for  instance,  in  severe  myocardial  weak- 
ness), the  hollows  above  the  clavicles  and  in  the  episternal 
become  more  pronounced  than  normal. 

In  addition  to  the  actual  ventricular  contraction,  another 
factor  is  concerned  with  the  fullness  or  emptiness  of  these 
hollows  of  which  we  are  speaking,  and  greatly  adds  to  the  im- 
portance of  carefully  noting  their  condition.  For  whenever 
(as  a  result  of  cardiac  failure  in  a  fairly  strong  heart)  there  is 
venous  plethora  the  abnormal  fullness  of  the  lungs  and  venous 
system  will  not  only  cause  a  lowering  of  the  diaphragm,  but 
the  same  abnormal  intrathoracic  pressure  will  cause  a  bulging 
of  the  areas  above  the  clavicles.  In  the  same  way  when, 
owing  to  grave  myocardial  weakness,  there  is  emptiness  of  the 
lungs  and  the  venous  system,  the  same  negative  pressure 
which  causes  the  diaphragm  to  rise  will  also  cause  an  indrawing 
of  the  tissues  in  the  supra-clavicular  spaces  and  the  episternal 
notch,  and  give  rise  to  a  deepening  of  the  hollows  of  which 
we  have  spoken.  Therefore,  we  can  by  palpation  of  the 
jugular  bulb  and  by  observation  of  the  general  fullness  above 


VENOUS  PHENOMENA  135 

the  clavicles  gain  important  information  as  to  the  fullness 
or  emptiness  of  the  auriculo-venous  reservoir  and  of  the  strength 
of  the  contraction  of  the  right  ventricle.  Although  the  fullness 
of  the  venous  system  and  the  increase  in  the  strength  of  the 
pulsation,  here  spoken  of  together,  are  usually  associated  clini- 
cally, it  is  not  necessarily  so  ;  and  sometimes  very  considerable 
fullness  of  the  veins  may  be  associated  with  a  weak  ventricular 
pulse,  and  when  this  is  so,  it  gives  an  important  indication  as 
to  the  state  of  the  circulation,  and  points  to  myocardial  weak- 
ness and  often  to  some  sudden  embarrassment  of  a  weak 
ventricle  ;  on  the  other  hand,  an  abnormally  strong  jugular 
pulse  may  be  unaccompanied  by  any  marked  over-filliag  of 
the  general  venous  system  of  the  thorax. 

When  dealing  with  the  veins  in  the  distal  side  of  the  valves 
which  guard  the  subclavian  and  innominate  veins,  there  are 
two  distinct  directions  in  which  we  have  to  gain  information. 

Firstly,  Are  the  veins  of  normal  fullness  or  are  they  fuller 
or  less  full  than  normal  ?  and,  secondly.  Is  there  any  evidence 
that  the  venous  valves  have  given  way  and  are  allowing  a  reflux 
of  blood  from  the  auriculo-venous  reservoir  into  them  during 
the  ventricular  systole  ? 

The  degree  of  fullness  of  the  veins  above  the  valves,  while 
not  giving  as  striking  evidence,  as  to  the  general  condition 
of  the  circulation,  as  is  obtained  from  the  reservoir  on  their 
proximal  side,  is  yet  of  importance  as  confirming  the  evidence 
thus  obtained  ;  but  so  far  as  positive  evidence  of  the  early 
occurrence  of  cardiac  failure  is  concerned,  the  evidence  is  of 
more  value  than  that  given  by  the  auriculo-venous  reservoir, 
because,  owing  to  their  accessiblity,  the  veins  give  evidence 
of  quite  shght  changes  in  the  effectiveness  of  the  work  of  the 
right  ventricle. 

So  far  as  concerns  the  negative  evidence  given  by  their 
emptiness,  this  is  of  but  little  value  as  compared  with  that  given 
in  other  ways,  as  already  described. 

As  regards  true  pulsation  in  the  veins  of  the  neck,  due  to 
tricuspid  regm-gitation,  it  does  not  at  the  present  time  seem 
possible  to  speak  definitely,  so  far  as  the  full  interpretation  of  the 
different  types  of  pulsation  is  concerned.  The  kind  of  pulsation 
varies  much  in  different  cases.    Sometimes  there  is  a  distinct 


136  LATER  LIFE 

double  beat  right  up  to  the  angle  of  the  jaw.  A  good  deal 
remains  to  be  done  by  the  careful  record  and  study  of  the  venous 
pulse  by  means  of  the  cardiograph  ;  for  the  writer  is  impressed 
by  the  fact  that  the  current  interpretation  of  venous  tracings 
is,  to  say  the  least,  somewhat  inadequate.  It  is  extremely 
likely  that  some  of  the  sudden  movements  seen  in  the  veins, 
as  recorded  by  the  cardiograph  are  really  due  to  a  true  con- 
traction of  the  muscular  walls  of  the  veins  themselves. 

With  a  fuller  knowledge  of  the  meaning  of  the  venous 
pulse,  we  shall  gain  a  fuller  knowledge  of  the  mode  of  action 
of  the  right  side  of  the  heart  under  the  varying  conditions 
which  disease  induces. 

We  must  now  go  a  little  more  into  detail,  with  regard  to 
the  information  we  can  obtain,  by  studying  the  veins  of  the 
neck.  The  subject  is,  however,  somewhat  difficult  to  deal 
with  concisely,  owing  to  the  complicated  nature  of  the  inter- 
relationships of  the  various  factors  concerned,  and  therefore 
anything  approaching  completeness  or  scientific  method  must 
not  be  expected. 

In  the  first  place,  a  simple  table  (see  pp.  137  and  138)  wiU 
be  given  showing  the  main  diagnostic  points  to  be  noted  in 
connection  with  the  state  of  the  veins  and  the  probable  inter- 
pretation of  the  various  groupings  of  the  phenomena  observed, 
and  then  some  rather  fuller  notes  upon  the  same  subjects  will 
be  given. 

Some  of  the  remarks  will  be  so  simple  as  to  be  self-evident, 
whereas  the  truth  of  others  may  appear  questionable  at  first 
sight,  although  experience  will  probably  prove  their  reliabihty 
in  most  instances. 

They  will  be  given  as  a  series  of  aphorisms. 

The  following  remarlis  illustrate  rather  more  fully  some  of 
the  points  to  which  attention  is  drawn  in  the  table. 

Fullness  of  the  neck  veins,  with  manifest  systolic  pulsation 
in  them,  suggests  a  strong  right  ventricle  working  against 
abnormal  resistance  to  the  circulation  through  the  lungs. 
The  commonest  cause  for  such,  interference  with  the  pulmonary 
circulation  is,  perhaps,  disease  of  the  mitral  or  aortic  valves. 

A  manifestly  excessive  carotid  pulsation  associated  with 
strong  pulsation  in  the  neck  veins  would  make  the  diagnosis 


VENOUS  PHENOMENA 


137 


Venous  Phenomena  of  Cardiac  Failure 


No. 
1 

Distension 
oE  veins 
of  neck 

False 
pulsation 

True 
pulsation 

Jugular 

bulb 
pulsation 

Diagnosis 

None 

None 

None 

Moderate 

Normal  circulation. 

strength 

2 

None 

None 

None 

Very 

strong  and 

full 

Failing  right  ventricle 
where  tricuspid  re- 
gurgitation is  en- 
tirely downwards  to 
tlie  Liver. 

3 

Some 

Some 
false 

None 

Normal 

Slight  right  ventricle 
failure.  General  di- 
latation, if  present, 
not  enough  to  cause 
tricuspid  regurgita- 
tion. In  the  heart 
failure  of  anaemia  in 
adolescence,  slight 
pneumonia,  &c. 

4 

Some 

Well 

SUght 

Too  full 

Some    general    dilata- 

marked 

or  none 

and  strong 

tion  of  right  ven- 
tricle and  com- 
mencing tricuspid 
regurgitation. 

5 

Well 

Present 

Some 

Too  full 

Some  tricuspid  regur- 

marked 

and  strong 

gitation. 

6 

Well 

Well 

Some 

Too  full 

Severe  embarrassment 

marked 

marked 

and  strong 

of  right  ventricle. 
Sudden  somewhat 
severe  pneumonia 
or  asthmatic  attack. 

7 

Well 

Little 

Well 

Too  full 

Considerable  tricuspid 

marked 

marked 

and  strong 

regiirgitation.  Con- 
siderable degree  of 
failure  of  left  ven- 
tricle from  valvular 
disease  or  overstrain. 

8 

WeU 

Little 

Strong 

Not 

Considerable  tricuspid 

marked 

or  none 

palpable 

regurgitation  with 
failure  of  venous 
valves.  Failing  com- 
pensation with  good 
heart  muscle. 

9 

WeU 

None 

Visible 

Feeble 

Onset      of      muscular 

marked 

but 

feebly 

palpable 

feebleness  complicat- 
ing tricuspid  regur- 
gitation. 

10 

Moderate 

None 

Feeble 

Feeble 

Weaker  muscle. 

11 

Little 

None 

None 

Very 
weak. 

Very  weak  muscles  of 
right  ventricle. 

12 

No  full- 
ness 

None 

None 

None 

Considerable  fatty 
degeneration  of  right 
ventricle. 

138  LATER  LIFE 

Venous  Phenomena  of  Cardiac  Failure — continued 


No. 
13 

Distension 
of  veins 
of  neck 

False 
pulsation 

True 
pulsation 

Jugular 

bulb 
pulsation 

Diagnosis 

Empty 

None 

None 

Small 

Degeneration    of    left 

and 

but  mod- 

ventricle with  mod- 

hollow- 

erate 

erately  strong  right 

ness  above 

strength 

ventricle. 

the 

clavicle 

14 

Empty 

and 

hollow- 

nes3  above 

the 

clavicle 

None 

None 

None 

Dangerously          weak 
heart   muscles   from 
intoxication  or  fatty 
degeneration. 

of  aortic  regurgitation  with  failing  compensation  almost  certain. 
The  association  of  increased  cardiac  dullness  to  the  right  of  the 
sternum  and  increased  pulsation  over  the  right  ventricle  just 
to  the  left  of  the  sternum,  with  strong  venous  pulsation,  would 
suggest  that  the  heart  was  distensible  ;  whereas  the  absence  of 
right  ventricular  dilatation  under  such  circumstances  would  be 
strong  evidence  that  the  heart  was  relatively  rigid. 

A  well-marked  systolic  impulse  in  the  neck  veins  without 
any  evidence  of  valvular  disease  would  suggest  some  inter- 
ference with  the  pulmonary  circulation  by  some  affection  of 
the  lungs  (emph^ysema,  for  instance),  or  the  recent  onset  of 
failure  of  the  left  ventricle  from  overstrain,  from  muscular 
weakness,  or  from  ineffective  action  such  as  is  associated 
with  certain  types  of  arythmia. 

Where  the  fullness  and  systolic  pulsation  are  only  moderate 
in  amount,  there  are  many  more  alternatives  than  when  both 
are  considerable.  In  such  cases,  the  following  generalisation 
can  be  made. 

Broadly  speaking,  it  can  be  asserted  that  muscular  weakness 
of  the  heart  can  be  diagnosed  whenever  well-marked  cardiac 
failure  is  associated  with  the  absence  of  well-marked  pulsation 
in  the  neck  veins,  whether  they  be  fall  or  empty,  always  pro- 
vided that  the  presence  of  tricuspid  regurgitation  downwards 
into  the  hepatic  vein  has  been  also  excluded. 

This  generalisation  can  also  be  carried  further  ;  for  it  is 
safe  to  consider  that  in  well-marked  heart  failure  the  degree 
of  weakness  of  the  pulsation  and  of  the  emptiness  of  the  veins 


VENOUS  PHENOMENA  139 

is  a  measure  of  the  degree  of  muscular  weakness  of  the  right 
ventricle  which  is  present. 

In  an  extreme  case,  gi'eat  dyspnoea  may  be  associated 
with  emptiness  of  the  neck  veins,  and  well-marked  hollows 
above  the  clavicle  and  in  the  episternal  notch.  Such  a  condi- 
tion will  point  to  the  presence  of  well-marked  fatty  degeneration 
of  the  right  ventricle.  This  diagnosis  will  be  confirmed  by 
weakness  of  the  right  ventricular  heart  sounds  and  the  absence 
of  any  cardiac  impulse  just  to  the  left  of  the  sternum  or  in  the 
epigastrium.  If  the  myocardial  weakness  involves  the  left  side 
as  well  as  the  right  its  sounds  will  be  feeble,  its  impulse  weak  or 
absent,  and  the  radial  pulse  will  also  give  evidence  of  the  fact. 

If,  on  the  other  hand,  the  degeneration  mainly  involves 
the  right  side  and  the  left  is  fairly  strong,  the  apex  impulse 
and  sounds,  and  the  radial  pulse,  may  all  be  fairly  strong. 
Sometimes,  indeed,  in  such  a  case  as  this  the  radial  pulse  may 
show  a  strong  wave  with  a  blood  pressure  as  high  as  160  mm. 
of  mercury,  although  the  patient  may  be  within  a  few  hours 
of  death. 

Moderate  fulhiess  of  the  neck  veins  and  moderate  pulsa- 
tion in  a  patient  with  valvular  disease  would  be  evidence 
that  compensation  was  not  very  unsatisfactory. 
\M  In  a  patient  with  a  dilated  left  ventricle  from  overstrain, 
the  meaning  of  moderate  fullness  and  pulsation  of  the  neck 
veins  would  depend  largely  upon  the  other  phenomena  present. 

For  instance,  with  a  history  of  increasing  breathlessness 
and  a  feeble  diffuse  apex  beat,  good  pulsation  in  the  veins 
of  the  neck,  when  associated  with  signs  of  some  overaction 
of  the  right  ventricle,  would  suggest  failure  of  the  left  side 
with  compensatory  overactivity  of  the  right,  and  would  call 
for  careful  stimulation  and  also  for  lessening  of  the  heart's 
load  by  lowering  the  blood  pressure  if  there  were  evidence 
that  an  increase  in  the  arterial  resistance  was  a  factor  in 
the  case. 

[  If,  on  the  other  hand,  moderate  fullness  and  pulsation 
of  the  neck  veins  were  associated  with  signs  of  a  moderately 
strong  right  ventricle  and  of  a  normally  strong  left  ventricle, 
the  venous  fullness  and  pulsation  might  give  no  special  indica- 
tion for  treatment,  but  be  simply  a  phenomenon  that  showed  the 
highest  level  of  efficiency  to  which  a  weak  heart  could  attain. 


UO  LATER  LIFE 

In  such  a  case  any  increase  in  the  feebleness  of  the  heart 
would  be  associated  with  the  disappearance  of  the  pulsation, 
and  a  return  of  strength  would  be  accompanied  by  its 
reappearance. 

This  is  a  point  which  must  be  remembered  when  dealing 
with  the  myocardial  failure  of  later  hfe,  both  as  regards 
diagnosis,  prognosis,  and  treatment ;  for  there  are  many  pitfalls 
in  connection  with  feeble  and  absent  pulsation  in  the  veins 
of  the  neck.  In  a  strong  right  ventricle  with  a  strong  left 
one,  there  is  sure  to  be  a  venous  plethora  mth  well-marked 
pulsation  whenever  the  left  ventricle  is  sufficiently  over- 
burdened. 

In  a  weaker  right  ventricle  with  a  strong  left  there  will 
be  well-marked  venous  plethora,  but  A\ith  weaker  systolic 
pulsation  in  them. 

In  myocardial  weakness  of  both  sides  of  the  heart  the 
amount  of  fullness  and  pulsation  will  be  proportional  to  the 
heart's  vigour. 

When  fullness  of  the  veins  is  accompanied  by  little  or 
no  pulsation  in  them  it  is  strongly  suggestive  of  the  fact  that 
the  right  ventricle  is  weaker  than  the  left. 

It  has  been  already  pointed  out  that  in  a  case  of  con- 
siderable muscular  feebleness,  with  empty  and  non-pulsating 
veins,  a  reappearance  of  fulhiess  and  of  pulsation  in  them  would 
be  a  sign  of  retm-ning  strength.  It  may  not  always  be  so, 
however,  as  in  the  followng  clinical  history.  Tliis  case  seems 
to  show  clearly  that  emptiness  of  the  venous  system  is,  in 
myocardial  weakness,  a  compensator}^  phenomenon,  and  that 
a  weak  heart  works  better  when  the  veins  are  empty  than 
when  they  are  of  normal  fullness. 

The  patient  was  a  lady  over  eighty  years  of  age,  who  suffered 
from  high  arterial  resistance  with  dilatation  of  the  left  ventricle 
and  an  amount  of  heart  weakness  that,  while  readily  causing 
breathlessness  and  fatigue  on  physical  or  mental  exertion, 
was  not  enough  to  prevent  her  from  going  up-  and  downstairs. 
In  spite  of  this  degree  of  activity  there  was  in  this  case  com- 
pensatory diminution  in  the  amount  of  blood  in  circulation. 
The  neck  veins  were  as  a  rule  not  at  all  fuU,  and  were  in  all 
probability  less  full  than  normal,  for  the  compression  of  the 


VENOUS  PHENOMENA  141 

veins  caused  by  the  application  of  the  armlet  of  the 
sphygmomanometer  always  caused  a  sense  of  breathlessness 
accompanied  by  deep,  often  sighing,  inspirations.  The  venous 
blood  supply  to  the  right  heart  being  so  limited  that  some 
embarrassment  resulted  when  the  venous  return  from  the 
arm  was  prevented.  In  this  patient  it  was  thought  that 
rehef  would  be  given  by  lowering  the  peripheral  resistance 
by  means  of  nitroglycerine,  and  after  a  few  half-minim  doses, 
there  was  marked  increase  in  the  fullness  of  the  neck  veins, 
showing  that  more  blood  was  passing  through  the  capillaries, 
and  also  the  application  of  the  armlet  no  longer  caused  dyspnoea, 
showing  an  increase  in  the  amount  of  venous  blood  available 
for  the  supply  of  the  right  ventricle  ;  but  the  patient's  con- 
dition was  made  worse.  She  was  more  breathless  on  exertion, 
and  it  was  evident  that  the  effect  of  the  vaso- dilatation  was 
to  supply  the  heart  with  more  blood  than  it  could  properly 
deal  with. 

Such  a  case  as  this  shows  how  complicated  is  the  problem 
which  we  have  before  us  in  hearts  that  are  muscularly  weak, 
and  especially  in  those  cases  where  there  is  high  blood  pressure 
and  increase  in  the  peripheral  resistance  in  the  arteries.  This 
patient  still  possessed  sufficient  distensibUity  of  the  right 
ventricle  to  give  useful  indications  for  treatment.  Any  over- 
stepping of  the  prescribed  limitations  as  regards  exertion  was 
apt  to  cause  the  appearance  of  pulsation  over  the  right  ventricle 
just  to  the  left  of  the  sternum,  and,  on  the  other  hand,  improve- 
ment was  associated  with  a  diminution  in  its  pulsation  and  also 
its  size,  as  w^as  shown  by  the  appearance  of  full  lung  resonance 
just  to  the  left  of  the  sternum  in  the  fom'th  interspace.  In 
another  patient  the  interpretation  of  these  physical  signs 
might  be  the  reverse  of  what  it  was  here,  so  far  as  the  size  of 
the  right  ventricle  is  concerned ;  for  the  diminution  in  size,  which 
here  showed  a  return  to  normal,  might  in  a  case  with  greater 
myocardial  weakness  mean  a  lessening  of  the  heart's  power  and 
be  accompanied  by  increased  dyspnoea  and  w^eakness. 

In  fact,  in  this  same  patient,  when  she  was  suffering  from 
an  attack  of  pneumonia,  the  absence  of  right  ventricular  pul- 
sation, combined  with  this  same  diminution  in  the  amount  of 
dullness  just  to  the  left  of  the  sternum,  was  a  sign  of  dangerous 
weakness  of  the  right  ventricle  {vide  p.  105). 


142  LATER  LIFE 

How   FAR    CAN    WE    ASCERTAIN    THE    PaRT   PlAYED    BY 

Arterial  Resistance  in  Cardiac  Failure  ? 

In  the  cardiac  failure  of  later  life  increased  arterial  resistance 
plays  a  very  important  part  in  consequence  of  the  frequent 
occurrence  of  abnormalities  of  peripheral  resistance  due  to 
arterial  disease  or  spasm.  In  any  given  case,  however,  it  is 
not  at  all  easy  to  appraise  at  its  proper  value  the  share  which 
such  increased  resistance  as  may  be  present  is  taking  in  bringing 
about  the  cardiac  failure.  In  the  earlier  decades  of  life  this 
was  not  so,  and  it  was  comparatively  easy  to  say  to  what 
degree  the  cardiac  failure  in  any  particular  case  was  due  to  a 
pathological  increase  in  the  blood  pressure. 

The  fact  that  the  part  played  by  increased  peripheral 
resistance  is  often  an  unknown  factor  in  our  cardiac  problem 
greatly  complicates  our  diagnosis,  whose  aim,  especially  in  the 
cardiac  failure  of  later  life,  is  to  ascertain  the  strength  of  the 
heart  muscle. 

Let  us  take  an  instance. 

The  symptoms  evidently,  let  us  suppose,  point  to  heart 
failure,  and  the  question  to  be  answered  is  this  :  Is  the  failure 
due  to  the  heart  being  called  upon  to  do  more  work  than  normal  ? 
or  is  the  failure  due  to  the  heart's  inability  to  do  what  may  be 
called  a  normal  amount  of  work  because  of  muscular  weakness  ? 
In  early  life  the  answer  to  this  was  easy,  because  the  heart 
was  so  distensible  that  the  yielding  of  its  wall  (i.e.  dilatation) 
would  at  once  give  evidence  of  any  abnormally  great  intra- 
ventricular pressure,  and  thus  show  whether  the  failure  was 
due  to  excess  of  work  or  to  muscular  weakness. 

In  later  life,  however,  the  problem  is  complicated  by  the 
indistensibility  of  the  heart  wall,  and  therefore,  before  being 
able  to  solve  our  problem,  we  must  know  either  what  the 
distensibility  of  the  heart  waU  is  or  else  what  the  arterial 
resistance  is  against  which  the  heart  is  working,  before  we  can 
decide  as  to  the  strength  of  the  heart  muscle.  In  every  case, 
we  want  to  know  what  the  strength  of  the  heart  muscle  is 
and  what  the  arterial  resistance  is  against  which  it  has  to 
work,  and  until  we  do  know  this,  we  cannot  properly  treat  the 
case  or  give  a  reasonably  accurate  prognosis.    We  are  too  apt 


RADIAL  PULSE  143 

when  we  meet  with  a  case  of  cardiac  failure  just  to  try  cardiac 
tonics  or  vascular  relaxants  without  really  having  taken  the 
mental  exertion  of  analysing  the  symptoms  and  signs  and 
weighing  up  the  evidence  for  and  against  muscular  weakness 
of  the  heart  wall.  The  distinction  between  a  strong  heart 
and  a  weak  one  is  fahly  easily  made,  even  in  the  absence  of 
cardiac  dilatation,  because  we  have  a  measure  of  its  strength  in 
the  loudness  of  the  sounds  and  the  amount  of  venous  engorge- 
ment and  pulsation.  The  absence  of  these  phenomena  will 
indicate  that  myocardial  weakness  plays  an  important  part 
in  the  cardiac  failure. 

We  shall  therefore  now  go  into  the  difficult  question  of 
how  far  it  is  possible  to  ascertain  what  part  increased  arterial 
resistance  plays  in  any  particular  case  of  heart  failure. 

Value  of  the  Eadial  Pulse  in  the  Diagnosis  of  Cardiac 
Failure  in  Later  Life 

As  has  already  been  stated,  the  condition  of  the  pulse 
is  often  a  most  unreliable  guide  in  dealing  with  the  heart  failure 
of  later  life,  except  in  the  case  of  marked  weakness.  There 
are  two  good  reasons  for  this.  Fiistly,  unless  the  character 
of  the  pulse  prior  to  the  onset  of  the  cardiac  failure  is  known, 
it  is  almost  impossible  to  be  sure  that  a  normal  or  moderately 
strong  pulse  is  not  after  all  a  greatly  weakened  high  pressm-e 
pulse,  and  therefore  a  sign  of  greatly  weakened  heart. 

Secondly,  it  is  not  at  all  easy  to  tell  from  the  character  of 
the  radial  pulse  what  the  condition  of  the  right  ventricle  is. 
It  is  not  very  uncommon  to  find  cases  with  a  dangerously 
weak  right  ventricle  in  whom  the  radial  pulse  is  fau-ly  strong 
and  good. 

The  main  problem  from  a  diagnostic  point  of  view  is 
however,  associated  with  the  question.  How  can  we  ascertain 
the  amount  of  work  which  the  heart  is  doing  so  far  as  the 
arteries  are  concerned  ? 

It  is  not  enough  to  recognise  that  the  pulse  tension  is 
high — as  judged  by  the  finger — or  that  the  blood  pressure  is 
high — as  judged  by  the  sphygmomanometer — unless  we  are 
able  at  the  same  time  to  say  from  our  previous  knowledge 


144  LATER  LIFE 

of  the  case  that  there  has  been  a  rise  in  the  blood  pressure  and 
that  therefore  there  is  reason  to  expect  that  the  attack  of 
cardiac  failure  which  we  have  before  us  is  probably  due  to  the 
extra  load  thus  thrown  upon  the  heart.  If  we  have  not  this 
previous  knowledge  as  to  the  condition  of  the  circulation, 
the  blood  pressure,  high  though  it  be,  may  yet  be  lower  than 
what  is  normal  for  the  patient,  and  the  cardiac  failure  may  be 
more  due  to  myocardial  weakness  than  to  abnormal  peripheral 
resistance.  It  is  quite  possible  that  in  such  a  case  the  right 
treatment  might  be  to  try  to  raise  a  blood  pressure  already 
at  the  level  of  170  mm.  or  180  mm.,  and  that  the  proper  nutri- 
tion of  the  heart  muscle  would  not  be  restored  till  this  was 
done. 

There  is  a  question  which  must  be  asked  in  this  connection 
— namely,  Is  it  not  likely  that  we  may  occasionally  meet  with 
cases  of  high  blood  pressure  which  are  compensatory  in  their 
nature  ?  Cases,  say,  where  there  is  so  much  narrowing  of  the 
coronary  arteries  (the  result  of  atheroma)  that  an  adequate 
supply  of  blood  will  not  pass  through  them  at  the  ordinary 
pressure,  and  where  in  consequence  the  blood  pressure  has  to 
be  abnormally  raised  by  vasomotor  activity  in  order  to  ensure 
the  proper  nutrition  of  the  heart  muscle.  In  such  a  case  as 
this  it  is  easy  to  see  how  disaster  would  follow  the  attempt 
to  lower  further  a  high  blood  pressure  which  had,  in  conse- 
quence of  the  onset  of  myocardial  failure,  already  dropped 
below  the  safe  level. 

The  question  illustrates  the  difficulty  of  the  problem  before 
a  man  who  sees  a  case  of  cardiac  failure  in  later  hfe  for  the 
first  time  and  has  to  interpret  the  phenomena  observable  in 
the  radial  pulse. 

For  the  solution  of  this  problem  some  assistance  can,  I 
think,  be  gained  by  the  sphygmomanometer  if,  in  addition 
to  noting  the  effect  of  the  rise  in  pressure  upon  the  pulse  alone, 
attention  be  also  directed  to  the  range  of  movement  of  the 
mercury  column  at  the  various  pressures  to  which  the  artery 
is  exposed,  or,  better  still,  by  noting  the  range  of  movement 
of  some  form  of  oscillometer  ;  for  by  this  means  w^e  can  tell 
whether  the  height  of  the  blood  pressure  is  determined  by  the 
strength  of  the  heart's  contraction  alone,  or  whether  the  heart 


ARTERIAL  RESISTANCE  145 

is  being  forced  to  beat  more  powerfully  than  would  otherwise 
be  the  case  owing  to  contraction  of  the  peripheral  vessels. 

To  take  the  latter  case  first. 

If  there  be  an  abnormal  amount  of  contraction  of  the 
peripheral  vessels  and  the  heart  is  strong  enough  to  respond 
to  it,  we  shall  find  that  the  range  of  oscillation  remains  at  its 
maximum  almost  up  to  the  point  which  we  call  the  systoHc 
pressure,  when  the  artery  is  so  compressed  that  the  blood  can 
no  longer  be  forced  past  the  point  of  compression.  Thus  sup- 
posing the  range  of  oscillation  is  2  mm.  of  mercury  and  the 
systoHc  pressm-e  is  150  mm.,  we  shall  find  that  at  146  or  148 
the  range  is  still  2  mm.  of  mercmy,  and  at  150  it  suddenly 
drops  to  1,  and  the  pulse  is  no  longer  felt  at  the  wrist,  showing 
that  the  heart  is  strong  enough  to  keep  up  a  full  volume  of 
blood  in  the  artery  as  long  as  it  can  force  any  blood  at  all 
past  the  compressed  point.  If,  on  the  other  hand,  the  range  of 
movement  gradually  lessens — say,  at  130  it  is  2  mm.,  at  138 
1|  mm.,  at  144,  1  mm.,  at  150,  1  mm. — ^we  should,  I  believe, 
be  justified  in  saying  that  the  state  of  the  arteries  was  not 
the  controlhng  factor  in  determining  the  height  of  the 
blood  pressure.  In  the  normal  heart  with  normal  arteries 
this  gradual  subsidence  in  the  range  of  oscillation  is  the 
rule. 

If,  therefore,  we  found  a  pulse  with  a  systolic  pressure  of  160 
or  170  mm.,  with  this  gradual  subsidence  in  the  range  of  oscilla- 
tion, we  should  be  justified  in  suspecting  that  it  was  a  case 
where  the  blood  pressure  was  below  what  was  normal  for  the 
individual  and  that  some  myocardial  weakness  was  present. 
In  such  a  case,  we  should  be  prepared  to  see  a  rise  in  the 
measm-ed  blood  pressure  as  soon  as  the  heart  regained  its 
strength  ;  moreover,  in  such  a  case,  we  should  be  careful  as  to 
the  administration  of  nitrites  for  fear  of  still  further  impairing 
the  nutrition  of  the  cardiac  muscle  by  further  lowering  a  blood 
pressure  that  was  already  abnormally  low.  If,  on  the  other 
hand,  we  found  that  the  full  range  of  oscillations  continued 
close  up  to  the  maximum  pressure  that  the  artery  would 
stand,  we  should  expect  to  see  benefit  result  from  the  use  of 
nitrites,  and  should  continue  om-  efforts  to  lower  the  blood 
pressure  until  we  found  that  the  type  of  oscillation  changed, 


146  LATER  LIFE 

thus  showing  that  the  heart  was  no  longer  working  against 
a  resistance  clue  to  contracted  peripheral  vessels. 

Assistance  will  also  be  given  by  watching  the  oscillations 
in  the  possible  cases  of  compensatory  high  blood  pressure, 
already  spoken  of ;  for  in  such  a  case  as  this  a  lowering  of  the 
blood  pressure  would  soon  make  it  clear  that  there  was  no  real 
interference  with  the  circulation  by  pathological  contraction 
or  rigidity  of  the  arteries.  The  study  of  the  oscillations  of 
the  pulse  would  soon  show  the  uselessness  of  trying  to  lower 
the  blood  pressure  in  such  a  case  as  this. 

These  are  only  given  as  tentative  suggestions,  because 
the  writer  has  not  studied  the  pulse  by  means  of  the  oscillo- 
meter for  more  than  a  few  months — a  time  too  short  for 
anything  approaching  certainty  in  so  complex  a  question,  and 
too  short  also  for  bringing  forward  many  cases  in  support 
of  the  suggestions  here  given. 

Other  illustrations  may  be  given  of  the  fact  that  in  these 
cases  of  myocardial  weakness  phenomena  connected  with 
the  arteries  may  have  the  reverse  meaning  to  that  which 
they  have  in  strong  hearts.  Take  for  instance  the  subject 
of  the  blood  pressure  in  cases  where  the  peripheral  re- 
sistance is  increased.  A  patient  is  perhaps  seen  with  a 
hard  pulse  and  a  blood  pressure  of  145  mm.  or  so.  There 
are  signs  of  a  labouring  ventricle — for  the  left  ventricular 
sounds  are  too  short  and  sharp  and  the  heart  is,  moreover, 
irregular — an  extra  systole  with  a  following  pause  occurring 
every  eighth  or  tenth  beat  for  a  time  with  intervals  of 
greater  regularity.  After  endeavouring  for  many  weeks,  by 
means  of  drugs  of  the  salicylate  class  and  by  diet,  to  lessen 
the  amount  of  the  peripheral  resistance,  and  also  by  tonics 
and  rest  to  improve  the  strength  and  nutrition  of  the  heart,  it 
was  somewhat  smprising  to  find  that  the  blood  pressure  which 
formerly  stood  somewhere  about  145  mm.  was  now  370  mm. 
or  more.  This  observation  by  itself  might  have  been  disap- 
pointing, but  it  was  qualified  by  the  fact  that  the  apex  beat 
was  stronger  and  more  locahsed  ;  the  heart  sounds  also  w^ere 
quieter,  less  jerky,  and  more  normal  in  character,  suggesting 
greatly  increased  strength,  so  far  as  the  left  ventricle  was 
concerned.     The  pulse,  too,  was  more  regular,  and  the  patient 


ESTIMATE  OF  RIGIDITY  U7 

rather  stronger  and  less  easily  tired.  The  pulse,  moreover, 
felt  softer  to  the  finger,  although  the  blood  pressure  was  higher. 
This  was  apparently  due  to  the  fact  that  the  pulse  was  less 
tense  between  the  beats,  and  emptied  in  a  more  normal  manner. 
Here  the  rise  in  blood  pressm-e  was  doubtless  the  result  of 
increased  cardiac  strength  due  to  improved  nutrition,  and 
was  therefore  a  good  sign  and  not  a  bad  one,  as  it  would  have 
been  had  it  occurred  in  a  heart  that  was  muscularly  strong. 

The  illustrations  here  given  are  sufficient  to  show  how 
little  we  really  know  as  to  the  proper  reading  of  the  arterial 
pulse  in  cases  of  heart  failure. 

Even  in  early  hfe  the  condition  of  the  pulse  may  be  mis- 
leading. For  instance,  it  is  probable  that  in  Graves's  disease 
the  arterial  dilatation  is  primary,  and  the  overaction  of  the 
heart  only  a  result  of  the  arterial  change. 

This  whole  subject  cannot  be  adequately  dealt  with  until 
our  knowledge  has  been  considerably  increased  by  the  careful 
study  of  the  range  of  oscillations  of  the  pulse,  and  in  other 
ways. 

How    FAR    CAN    WE    ASCERTAIN    THE    DbGREE    OF    ElGIDITY 

OF  THE  Heart  Wall  ? 

When  speaking  of  the  problem  which  faces  us  in  dealing 
with  heart  failure  in  adult  and  later  life  mention  was  made  of 
the  fact  that  we  have  an  equation  with  three  unknown 
quantities — namely,  strength  of  heart  muscle,  arterial  resistance 
against  which  the  heart  is  working,  and  the  resisting  power  of 
the  heart  wall,  and  to  solve  the  equation  we  must  ascertain  the 
value  of  two  out  of  the  three  unknown  quantities. 

The  question  we  will  now  try  to  answer  is  :  Have  we  any 
means  of  estimating  the  resisting  power  of  the  cardiac  wall  ? 

In  certain  cases  it  is  easy.  For  instance,  where  we  find 
heart  failure  accompanied  by  distended  veins  or  enlarged 
liver  with  a  strong  pulsation  in  the  jugular  bulb  with  com- 
mencing cedema  of  the  ankles  associated  with  a  heart  sho^^ing 
no  evidences  of  dilatation,  we  shall  be  safe  in  saying  that 
the  cardiac  wall  possesses  abnormal  powers  of  resistance  to 

l2 


148  LATER  LIFE 

dilatation.  In  such  a  case  the  cardiac  strength  is  good,  and 
therefore  the  cause  of  failure  must  be  sought  for  elsewhere. 
The  value  of  two  of  our  three  unknown  quantities  are 
ascertained,  and  we  can  therefore  find  the  third,  as  follows  : — 

The  failure  may  be  due  to  valvular  disease  or  some  other 
easily  recognisable  cause,  or  it  may  be  due  to  some  condition 
such  as  adherent  pericardium  hampering  the  action  of  the 
heart.  These  points  can  be  decided  with  a  fair  degree  of 
certainty.  In  the  absence  of  any  such  cause  as  these,  w-e  can  in 
Buch  a  case  feel  reasonably  certain  that  the  arterial  system 
is  to  blame,  and  in  the  absence  of  any  signs  of  abnormal 
resistance  in  such  arteries  as  the  radial,  we  must  suspect 
rigidity  of  the  first  part  of  the  aorta  and  search  for  signs 
of  this  condition. 

Again,  in  a  condition  such  as  one  of  the  forms  of  valvular 
disease,  which  is  usually  associated  with  dilatation  and  hyper- 
trophy, the  absence  of  enlargement,  if  associated  with  the 
signs  of  good  muscular  strength,  would  also  justify  the 
diagnosis  of  an  abnormally  rigid  heart  wall  {vide  p.  433). 

In  cases,  however,  where  the  heart  was  weak  as  w'ell  as 
being  either  of  normal  size,  or  small,  the  question  as  to  the 
presence  of  abnormal  rigidity  would  not  be  so  easily  answered. 
In  a  case  of  cardiac  failure  accompanied  by  evident  signs  of 
muscular  weakness,  the  occurrence  of  attacks  of  angina  in  the 
absence  of  evidences  of  increased  arterial  resistance  would 
suggest  that  the  heart  wall  was  miduly  resistant,  and  by  its 
powers  of  mechanical  elasticity  was  apt  to  draw  into  the 
left  ventricle  a  larger  amount  of  blood  than  the  heart  muscle 
had  the  power  of  expelling.  In  such  a  case  as  this  nitrites 
would  have  to  be  used  with  caution,  because  by  increasing 
the  permeability  of  the  capillaries  and  therefore  the  fullness 
of  the  veins,  they  would  increase  the  risk  of  the  heart  over- 
filling itself  {vide  p.  140).  In  many  cases  with  weak  heart 
muscle  it  is  not  at  all  easy,  if  not  impossible,  to  form  any 
rehable  estimate  as  to  the  degree  of  rigidity  of  the  heart  wall. 
In  this  coimection  attention  may  be  drawn  to  the  follow- 
ing line  of  argument.  A  class  of  case  described  was  at  p.  87 
where  heart  failure  could  clearly  be  seen  to  occur  in  a  strong 


ESTIMATE  OF  RIGIDITY  149 

heart  with  resistant  walls,  because  venous  plethora  and  loud 
heart  sounds  were  unaccompanied  by  any  dilatation.  A  clinical 
group,  therefore,  exists  in  which  heart  failure  without  enlarge- 
ment occurs,  accompanied  by  venous  plethora  and  loud  heart 
sounds.  But  any  chnical  observer  can  also  convince  himself 
of  the  fact  that  cases  are  often  met  with  where  heart  failure 
without  enlargement  is  accompanied  by  emptiness  of  the  veins 
and  weak  heart  sounds.  The  recognition  of  these  two  types 
of  case  as  clinical  certainties  forces  upon  us  a  startling  and 
disconcerting  fact — namely,  that  cases  of  an  intermediate 
nature  must  sometimes  be  met  with,  and  that  therefore  we 
must  sometimes  come  across  cases  of  moderately  rigid  hearts 
with  failing  heart  muscle,  where  well-marked  heart  failure 
occurs,  associated  with  a  heart  of  normal  size  with  normal 
fuUness  of  the  veins  and  sounds  of  normal  loudness. 

In  view  of  the  fact  that  the  radial  pulse  may  be  quite  un- 
reliable for  purposes  of  estimating  heart  failure,  we  are  face 
to  face  with  the  uncomfortable  fact  that  we  may  occasionally 
meet  with  a  case  of  heart  failure  where  we  can  gain  no  help 
at  all  from  physical  examination,  because  the  heart  appears 
quite  normal,  and  we  must  therefore  depend  entirely  upon 
symptoms.     The  analysis  of  such  a  case  would  be  as  follows : — 

1.  Abnormal  arterial  resistance  accompanied  by  sufficient 
muscular  failure  to  reduce  the  high  tension  pulse  to  one  of 
apparently  normal  character. 

2.  A  muscularly  weak  and  rigid  left  ventricle  only  able 
to  respond  to  this  increased  resistance  by  developing  a  normal 
(and  therefore  inadequate)  intraventricular  pressure.  A  weak 
right  ventricle  also  only  able  to  develop  a  normal  and  therefore 
inadequate  pressure,  and  the  veins  would  therefore  have  a 
normal  degree  of  fullness. 

Such  a  heart  might  improve  in  one  of  two  ways.  Either 
it  might  gain  a  little  strength  with  the  result  that  the  sounds 
would  become  abnormally  loud  and  the  veins  overfull,  or  else 
if  the  left  ventricle  could  compensatorily  diminish  the  degree 
to  which  it  filled  itself,  the  heart  sounds  would  remain  of  the 
same  loudness,  but  the  blood  volume  would  diminish,  the 
veins  become  more  empty,  the  diaphragm  rise,  and  the  hver 
dullness  diminish.    On  the  occurrence  of  this  latter  sequence  of 


150  LATER  LIFE 

phenomena,  the  heart  would  once  more  be  able  to  carry  on 
the  circulation  fairly  well,  and  the  dyspnoea  on  exertion  would 
diminish  to  some  extent. 

What  has  just  been  said  points  to  one  answer  to  the  question  : 
How  can  we  recognise  the  presence  of  rigidity  of  the  heart 
wall  in  a  very  weak  heart  ?  We  can  say  this.  W^hen  we 
find  evidences  of  decided  weakness  of  the  heart  muscle  (breath- 
lessness,  faintness,  anginal  pain  on  exertion,  leg  pains  on 
walking,  &c.)  associated  with  a  heart  of  normal  size  (and  not 
smaller  than  normal),  and  with  signs  that  the  thoracic  viscera 
contain  the  normal  amount  of  blood  (i.e.  that  there  is  no 
compensatory  diminution  in  the  volume  of  blood  in  circulation 
proportionally  to  the  muscular  weakness),  we  are  justified  in 
assuming  rigidity  of  the  heart  wall,  and  if  we  are  wise,  we  shall 
caution  the  patient,  realising  that  he  is  running  a  grave  risk 
of  sudden  death. 

This  question  of  the  degree  of  rigidity  of  the  heart  wall 
is  one  of  much  practical  importance  in  later  fife,  and  is  often 
one  of  considerable  difiiculty.  We  often  meet  with  hearts 
that  have  not  dilated  under  conditions  of  overstrain  that 
might  reasonably  have  been  expected  to  produce  dilatation. 
The  question  which  has  then  to  be  answered  is  this  :  Are  we 
dealing  with  a  heart  with  fair  strength  and  an  unduly  rigid 
wall,  or  are  we  dealing  with  a  heart  ^vith  walls  of  normal  rigidity, 
but  with  such  a  deficiency  of  muscular  power  that  it  is  unable 
to  develop  enough  force  to  over -distend  them  ?  If  the  former, 
it  will  be  a  '  strong  heart  with  rigid  walls,'  and  we  have  already 
shown  the  points  whereby  such  a  heart  can  be  recognised.  If 
the  latter,  it  will  be  a  case  of  weak  heart  without  enlargement, 
and  we  must  look  for  signs  of  weakness  and  of  emptiness  of 
the  vascular  system — along  the  lines  already  given. 

Evidences  of  Eigidity  in  Cases  of  Valvular  Disease 

The  principles  already  laid  down  applj^  in  this  case  also, 
for  if  we  have  an  amount  of  dilatation  and  hypertrophy 
less  than  that  which  might  reasonably  be  expected  from  the 
amount  of  valvular  regurgitation  present,  we  are  justified  in 
diagnosing  undue  rigidity  of  the  heart  wall,  provided  that  the 


ESTIMATE  OF  RIGIDITY  151 

heart  does  not  show  signs  of  marked  muscular  weakness.  In 
such  a  case  as  this,  pronounced  pallor  will  accompany  such 
indistensibility,  as  is  pointed  out  in  the  essay  dealing  with  that 
subject  (see  p.  450). 

As  regards  the  means  of  judging  as  to  the  amount  of  mitral 
regurgitation  by  the  extent  to  which  the  murmur  is  conducted 
down  the  spine  {vide  Essay,  p.  442),  and  of  aortic  regurgita- 
tion by  the  amount  of  pulsation  of  the  carotid  arteries  {vide 
p.  347),  we  must  be  able  to  form  some  idea  as  to  the  amount  of 
regm'gitation  before  we  can  say  that  dilatation  and  hypertrophy 
are,  or  are  not,  adequate. 

There  are  one  or  two  minor  points  in  connection  with  the 
examination  of  the  heart  which  had  better  be  referred  to, 
although  they  are  but  common-sense  points,  known  to  every 
clinician. 

When  deahng  with  an  area  of  cardiac  dullness  that  is 
apparently  of  less  than  the  normal  size,  we  must  make  certain, 
firstly,  that  the  diminution  is  not  due  to  simple  over-lapping 
by  lungs  more  voluminous  than  usual,  and,  secondly,  granted 
that  the  lungs  are,  to  all  appearance  normal,  we  must  make 
sure  that  there  is  no  evident  reason,  other  than  its  want  of 
its  proper  fullness  and  rigidity,  for  the  heart  falling  back, 
away  from  the  chest  wall.  The  variation  noticeable  in  the 
mobility  of  the  heart  in  different  healthy  individuals  must 
not  be  forgotten. 

The  possibility  also  of  shrinkage  of  a  portion  of  one  lung 
as  the  result  of  disease,  with  such  a  measure  of  recovery  as  to 
make  the  evidences  of  it  very  slight,  must  not  be  forgotten,  for 
this  might  either  cause  falling  back  of  the  heart  or  else  possibly 
the  simulation  of  enlargement  by  its  being  less  covered  than 
normally  by  the  lungs. 

Also  as  regards  the  recognition  of  enlargement,  we  must  be 
careful  to  make  our  examination  of  the  heart  thorough,  or  we 
may  be  caught  napping,  as  the  able  general  practitioner  was, 
who  brought  the  patient  whose  case  is  detailed  at  p.  374  to  see  me. 
In  this  case  the  practitioner  was  impressed  by  the  lady's 
breathlessness  on  exertion,  and  by  the  fact  that  her  apex  beat 
was  in  the  axilla,  and  diagnosed  cardiac  failure  and  dilatation ; 
but,  through  not  percussing  out  the  heart,  failed  to  notice  that 


152  LATER  LIFE 

the  right  border  of  the  heart  was  well  to  the  left  of  the  sternum, 
and  that  the  heart  was  not  really  as  much  enlarged  as  it 
appeared  to  be,  but  was  simply  displaced  into  the  left  axilla 
by  the  gradual  and  unobserved  collapse  of  the  left  lung,  and 
the  crossing  of  the  right  one,  which  resulted  from  an  almost 
symptomless  but  destructive  form  of  tuberculosis. 

Or  take  another  case,  such  as  that  mentioned  at  p.  365, 
where  a  man  with  mitral  stenosis  has  an  apex  beat  in  the  seventh 
interspace  well  external  to  the  nipple  line.  Extreme  dilatation 
of  the  left  ventricle  would  naturally  be  diagnosed :  but  a  careful 
examination  of  the  chest  would  show  that  the  diaphragm  was 
very  low,  and  that  the  pulmonary  second  sound  was  heard  best 
at  about  the  level  of  the  fourth  rib,  instead  of  in  the  second 
interspace.  Also  that  the  area  of  cardiac  dullness  was  lower 
than  natural — in  other  words,  this  was  simply  a  case  of  dowTi- 
ward  displacement  of  the  heart.  The  displacement  was  con- 
firmed by  a  radiograph  (as  is  shown  in  Plate  VI).  The  patient 
had  suffered  from  a  greatly  obstructed  mitral  valve  for  twenty 
years,  and  the  chronic  venous  distension  of  long  standing 
had  through  persistent  over-filling  of  the  heart  and  vessels  in 
the  thorax,  brought  about  a  downward  displacement  of  the 
diaphragm,  which  naturally  caused  a  dropping  of  the  heart 
also. 

Another  simple  point  in  connection  with  the  examination 
of  the  heart  is  this.  In  muscular  weakness  we  have  to  depend 
a  good  deal  upon  the  degree  of  feebleness  of  the  cardiac  sounds, 
therefore  we  shall  have  to  look  very  carefuUy  for  the  presence 
of  any  conditions  other  than  cardiac  weakness  that  may  modify 
the  loudness  of  the  heart  sounds.  The  presence  of  emphysema 
and  its  amount  must  be  carefully  noted  as  well  as  the  amount 
to  which  the  heart  is  covered  by  lung  when  there  is  no 
emphysema.  The  amount  of  fat  on  the  chest  wall  must  also 
be  noted  and  its  effect  estimated. 

As  regards  the  evidence  given  by  the  size  of  the  liver  dullness, 
we  must  remember  that  causes  other  than  cardiac  failure  will 
lead  to  its  diminution,  as  is  described  in  Essay  III.  Other 
causes  for  diminution  in  the  size  of  the  liver  dullness  must 
therefore  be  excluded  before  we  lay  stress  upon  that  diminution 
in  connection  with  cardiac  diagnosis.     Similarly,  where  there 


DIAGNOSTIC  DIFFICULTIES  153 

is  no  diminution  there  may  be  a  history,  which  would  suggest 
cirrhosis,  or  something  else,  that  would  render  unlikely  the 
changes  which  we  have  associated  with  heart  failure. 

While  speaking  of  the  liver,  it  may  be  well  once  more  to 
draw  attention  to  a  somewhat  new  and  important  observation 
— namely,  that  percussion  is  not  always  a  reliable  guide  to  the 
actual  size  of  the  liver,  and  especially  for  the  type  of  enlargement 
which  is  associated  with  heart  failure  where  the  right  ventricle 
is  fairly  strong.  As  is  pointed  out  (pp.  24  and  192),  tense  liver 
tissue  appears  to  possess  to  an  abnormal  degree  the  power 
of  conducting  percussion  and  sound  vibrations,  and  thus  a 
resonant  note  may  be  obtained  through  an  abnormal  thickness 
of  liver  tissue. 

It  is  therefore  quite  possible  in  a  somewhat  hasty  examina- 
tion to  miss  the  fact  that  the  liver  is  enlarged.  In  such  a  case, 
however,  it  is  always  possible  to  feel  the  edge,  and  it  is  no 
unusual  thing  to  iind  that  there  is  a  fully  resonant  note  for 
one,  two,  or  even  three  inches  above  the  level  at  which  the 
edge  is  felt. 

fe'  While  at  work  on  this  section,  the  writer  saw  a  case 
where  in  typhoid  enlargement  of  the  liver  there  was  a  good 
resonant  note  for  two  inches  or  more  above  the  level  at  which 
the  edge  was  felt. 

Difficulties  in  Diagnosis  due  to  one  Ventricle  being 
Weak  while  the  other  is  Strong 

We  now  have  to  discuss  a  diagnostic  difficulty  which  is 
associated  with  one  of  the  most  marked  differences  between  the 
heart  in  early  and  in  later  life — namely,  the  fact  that,  whereas 
in  early  hfe  the  common  causes  of  myocardial  weakness  are 
general  causes,  such  as  the  poisons  of  infective  disease,  the 
commonest  causes  of  myocardial  weakness  in  later  life  are  local 
and  are  due  to  interference  with  the  blood  supply  to  the  heart. 
This  being  the  case,  we  are  prepared  for  the  fact  that  one  of  the 
two  coronary  arteries  may  be  more  interfered  with  by  disease 
than  the  other,  and  that  therefore  the  nutrition  of  one  ventricle 
may  suffer  more  than  the  other. 

In  all  our  cases  of  myocardial  weakness,  therefore,  in  later 


154  LATER  LIFE 

life,  we  shall  do  well,  in  studying  the  symptoms  and  physical 
signs,  to  separate  those  which  mainly  depend  upon  the  right 
ventricle  from  those  which  concern  the  left,  in  order  that  we 
may  be  able  to  form  a  judgment  as  to  whether  the  patient's 
symptoms  are  due  to  the  failure  of  one  ventricle  more  than 
the  other,  or  whether  both  are  equally  affected. 

Firstly,  as  far  as  regards  the  general  symptoms.  Breath- 
lessness  is,  as  already  pointed  out,  apt  to  be  the  prominent 
symptom  in  cases  where  the  right  ventricle  is  weak  ;  whereas 
when  the  left  is  the  weak  one,  faintness  and  weariness  and 
general  weakness  are  more  prominent.  Faintness  is  of  com'se 
apt  to  occur  when  the  right  ventricle  is  weak,  owing  to  its 
inability  to  send  on  the  proper  amount  of  blood  through  the 
lungs  for  the  full  supply  of  the  left  side  of  the  heart. 

But  the  fainting  attacks  in  weak  right  ventricle  are  less 
frequent  than  in  the  case  of  the  left,  and  I  think  it  will  be 
found  that  frequent  '  faint  feelings  '  and  shght  attacks  of 
vertigo  of  cardiac  origin  may  be  accepted  as  showing  myo- 
cardial failure  of  the  left  ventricle. 

The  physical  signs  need  not  be  gone  into  fully,  for  they  have 
been  already  dealt  with  seriatim  ;  but  it  must,  however,  be 
remembered  that  a  strong  right  ventricle  may  be  associated 
with  a  weak  left  one,  or  vice  versa,  and  we  may,  as  in  the 
clinical  history  shortly  to  be  given,  be  surprised  at  a  patient 
who  usually  has  a  good  pulse  dying  in  a  fainting  attack. 

With  a  strong  right  ventricle  there  is  more  apt  to  be  fullness 
of  the  veins  ;  but  I  think  it  will  be  found  that  whenever  there 
is  marked  weakness  of  one  ventricle — no  matter  which — the 
characteristic  compensatory  diminution  in  the  amount  of 
blood  in  active  circulation  does  take  place. 

To  illustrate  the  subject,  I  propose  to  give  one  or  two 
clinical  histories. 

The  first  case  is  that  of  a  woman  aged  sixty-one,  who  was 
admitted  to  the  hospital  for  breathlessness.  She  had  been  short 
of  breath  for  several  years,  and  of  late  had  been  gradually  getting 
worse.  Eecently,  she  had  rapidly  got  weaker,  and  the  day 
before  admission,  she  had  a  serious  fainting  attack — the  first 
of  the  kind  she  had  had. 

There  was  no  history  of  any  previous  illnesses,  and  her 


DIAGNOSTIC   DIFFICULTIES  155 

present  condition  had  developed  gradually.  Her  state  on 
admission  was  as  follows  :  A  rather  stout  woman,  very  pale, 
not  breathless  when  lying  in  bed  with  a  moderately  high 
bed  rest,  but  breathless  on  exertion  and  unable  to  lie  flat  in 
bed.     There  was  no  dropsy  and  no  cyanosis. 

The  pulse  was  decidedly  small  but  of  good  strength,  and 
was  of  the  strikingly  collapsing  character  usually  associated 
with  aortic  regurgitation.  Although  its  volume  was  small 
it  came  up  under  the  finger  with  suddenness  and  force  and 
subsided  again  with  equal  suddenness,  leaving  the  artery 
empty  to  the  touch  between  the  heart  beats.  On  testing 
it  with  the  Kiva  Eocci  sphygmomanometer,  it  was  found  that 
the  pulse  wave  would  withstand  a  pressure  of  nearly  160  mm. 
of  mercury.  On  testing  the  collapsibihty  of  the  pulse  when 
the  arm  was  raised  or  lowered,  it  was  found  that  elevation 
of  the  arm  did  not,  as  in  aortic  regurgitation,  increase  the 
collapsing  character  of  the  pulse.  On  looking  at  the  neck 
there  was  not  only  no  pulsation  of  the  veins,  but  there  was 
a  hollowing  above  the  clavicles  which  suggested  undue 
emptiness  of  the  vessels. 

As  regards  the  heart  there  was  no  visible  or  palpable 
impulse  anywhere,  and  the  cardiac  area  was  small — decidedly 
less  than  normal — and  the  liver  was  not  enlarged.  The  cardiac 
sounds  were  decidedly  weak  and  there  was  no  murmur. 

The  lungs  and  other  organs  appeared  quite  healthy.  This 
patient  was  evidently  suffering  from  weakness  of  the  heart 
muscle  of  a  very  severe  degi-ee,  for  the  heart  had  not  sufficient 
strength  to  keep  the  superior  cava  and  neck  veins  distended 
and  pulsating. 

The  diagnosis  was  heart  weakness  due  to  fatty  degenera- 
tion— the  result  probably  of  diseased  coronary  arteries.  A 
more  complete  analysis  of  the  symptoms  would  have  led  to 
an  even  fuller  diagnosis  ;  but  the  importance  of  the  collapsing 
pulse,  and  the  systohc  pressure  of  160  mm.,  coupled  with  the 
empty  veins,  was  not  recognised  till  after  the  post-mortem 
revealed  the  true  nature  of  the  case. 

The  patient  was  given  small  doses  of  strophanthus  and 
strychnine,  and  seemed  to  be  improving,  when  suddenly 
she  had  another  fainting  attack  five  days  after  admission, 
and  died  a  few  hours  later  in  a  second  attack.  The  earlier 
of  the  two  attacks  came  on  at  4  p.m.  There  was  marked 
dyspncBa  and  cyanosis  with  pain  over  the  heart  and  left 
chest,  and  the  pulse  was  almost  imperceptible.     She  rallied 


156  LATER  LIFE 

somewhat,  but  became  worse  an  hour  later.  In  this  second 
attack  she  suddenly  sat  up  in  bed,  and  then  fell  back  dead. 
At  the  post-mortem  there  was  found  to  be  fatty  degeneration 
of  the  right  ventricle,  due  to  atheroma  blocking  its  coronary 
artery.  The  condition  of  the  muscular  wall  of  the  left 
ventricle  was  good,  and  the  coronary  artery  supplying  it  was 
not  interfered  with  by  disease. 

Here,  then,  was  the  explanation  of  the  small  powerful 
collapsing  pulse. 

The  right  side  of  the  heart  was  too  feeble  to  force  the 
proper  amount  of  blood  through  the  lungs,  and,  as  the  con- 
dition had  evidently  developed  slowly,  the  amount  of  blood 
in  circulation  had  presumably  diminished  yari  passu  with  the 
diminution  in  the  strength  of  the  right  ventricle,  thus  leading 
to  no  venous  plethora,  as  might  have  been  expected  had  the 
failure  of  the  right  ventricle  been  less  gradual. 

The  left  ventricle  was  therefore  underfilled  at  each  beat, 
and,  in  order  to  get  as  large  an  amount  as  possible  into  the 
capillaries  of  the  brain  and  elsewhere,  the  blood  was  thrown 
out  of  the  ventricle  suddenly  and  with  force,  the  arteries  being 
kept  as  contracted  as  possible. 

The  rapid  collapse  of  the  pulse  wave  and  the  emptiness 
of  the  artery  between  the  beats  were  due  to  the  abnormally 
small  volume  of  blood  causing  the  pulse  wave. 

This  case  illustrates  well  the  main  signs  upon  which  diag- 
nosis of  a  fatty  right  ventricle  with  a  fauly  strong  left  ventricle 
are  to  be  based — namely,  great  dyspnoea  and  weak  right 
ventricular  sounds,  coupled  with  absence  of  well-marked  venous 
pulsation  in  the  neck  in  combmation  with  a  regular  and  not 
very  rapid  pulse  of  small  volume  but  fair  strength.  Where 
some  amount  of  arterio-sclerosis  is  present,  the  rapid  and  great 
collapse  of  the  pulse  may  not  be  noticeable ;  but  where 
present,  as  in  the  case  here  noted,  its  diagnostic  importance 
is  great. 

The  prognosis,  it  is  needless  to  add,  is  in  such  a  case 
extremely  gi'ave. 

The  following  case  is  one  where  the  diagnosis  of  fatty  or 
fibroid  degeneration  involving  mainly  the  right  ventricle  was, 


DIAGNOSTIC  DIFFICULTIES 


157 


in  the  writer's  opinion,  justified  by  the  symptoms,  although  it 
was  not  verified  by  a  post-mortem,  as  the  patient  recovered 
sufficiently  to  go  home.  The  patient  was  a  jobbing  gardener, 
sixty  years  of  age,  who  was  suffering  from  emphysema,  cardiac 
weakness,  and  some  nephritis. 

His  lungs  were  not  in  a  very  bad  condition,  and  his  nephritis 
did  not  seem  to  be  causing  much  trouble. 

His  main  complaint  was  breathlessness.     He  had  been  ailing 

Myocardial  Weakness  mainly  involving  the  Right  Venteicle 


Fig.  20. 

H.    H.,    aged     sixty.      Weak 
ventricle;    stronger  left  one. 


Fig.  21. 

right  H.  H.,  aged    sixty,  June  14,  1911. 

Heart  stronger ;  cardiac  area  larger. 


eight  years— at  first  mainly  with  cough,  due  probably  to  chronic 
bronchitis— and  for  years  he  had  had  dyspnoea  on  exertion. 
Within  the  last  six  weeks  prior  to  admission  to  hospital,  dropsy 
of  the  ankles  had  come  on.  He  had  been  continuing  to  work 
two  days  a  week  till  within  a  short  time  of  coming  to  hospital, 
in  spite  of  his  breathlessness  being  so  bad  that  in  walking  to 
and  from  work  it  was  his  custom  to  rest  at  each  lamp-post  as 
he  came  to  it  in  order  to  get  his  breath.  Also  when  digging 
and  doing  similar  hard  work,  he  would  have  to  stop  and  wait  to 
get  his  breath  every  few  minutes.  When  he  found  that  his 
breathlessness  did  not  admit  of  his  walking  as  far  as  from  one 
lamp  to  the  next,  he  thought  it  was  time  for  him  to  come  to 
the  hospital,  and  he  was  admitted.     When  first  seen,  there  was 


158  LATER  LIFE 

well-marked  cyanosis  and  some  dropsy  of  the  legs  (of  which  the 
kidney  disease  may  have  been  a  contributory  cause).  There 
was  no  abnormal  distension  and  very  shght  pulsation  of  the 
veins  of  the  neck,  and  although  they  were  moderately  full  the 
supraclavicular  fossae  were  distinctly  hollow. 

There  was  no  dilatation  of  the  heart  to  the  right,  and  the 
cardiac  dullness  was  somewhat  diminished  in  area.  There  was 
no  absolute  dullness  except  a  little  in  the  fifth  interspace,  and  the 
relative  dullness  barely  reached  to  the  left  edge  of  the  sternum. 
The  absolute  liver  dullness  was  small  and  did  not  reach  to  the 
costal  arch. 

There  was  no  cardiac  impulse  to  be  felt,  and  the  apex  was 
probably  in  the  fifth  interspace  about  midway  between  the 
nipple  fine  and  the  anterior  axillary  line.  The  heart  sounds 
were  short  and  wanting  in  tone  over  both  right  and  left  ventricle, 
and  no  murmurs  were  present.  The  diagram  shown  in  fig.  20 
was  taken  about  a  fortnight  after  admission  when  his  cyanosis 
and  dropsy  had  gone,  and  his  dyspnoea  was  much  less  ;  but 
it  shows  the  heart  in  much  the  same  condition  as  on 
admission. 

Here  we  have  marked  cardiac  failure — as  judged  by  his 
great  dyspnoea  on  exertion  associated  with  no  abnormal  full- 
ness of  the  veins,  a  small  liver,  and  the  right  side  of  the  heart 
if  anything  smaller  than  normal.  There  was  a  considerable 
amount  of  emphysema  ;  for  there  was  very  little,  if  any,  true 
expansion  of  the  thorax,  and  the  upper  edge  of  the  fiver 
was  a  little  low,  and  breathlessness,  if  due  to  this  cause, 
ought  to  have  been  associated  with  an  over-full  venous 
system  and  a  labouring  right  heart  with  loud  sounds  and 
a  distended  liver. 

Here  we  have  clear  evidence  of  muscular  weakness  of 
the  right  ventricle,  and,  as  a  further  comment  upon  what  has 
recently  been  said,  it  might  be  added  that  the  evidence  was 
against  there  being  any  very  marked  rigidity  of  the  heart 
wall,  for  the  foUowing  reasons  :  The  ventricle  was  smaller 
than  normal,  Avhich  suggested  the  probability  that  it  had 
diminished  in  size  somewhat,  proportionally  to  the  lessened 
amount  of  blood  it  was  able  to  expel,  and  also  there  was  some 
variation  from  time  to  time  in  the  size  of  the  cardiac  area,  as 
shown  in  the  second  diagram,  which  was  taken  when  the  heart 


DIAGNOSTIC  DIFFICULTIES  159 

was  a  good  deal  stronger,  and  shows  some  increase  upward*? 
of  the  cardiac  area  as  compared  with  the  former  one. 

And  now  as  regards  the  left  ventricle.  It  is  evident  that 
the  left  side  was  fairly  strong,  otherwise  he  could  not  have 
continued  working  for  many  weeks — if  not  months— in  spite 
of  very  considerable  dyspnoea.  This  statement  is  also 
supported  by  the  condition  of  the  pulse,  which  was  hard  and 
wiry  ;  and  on  testing  mth  the  sphygmomanometer  was  found 
to  withstand  a  pressure  of  230  mm.  of  mercury.  The  arterial 
wall  was  not  specially  hard,  and  the  pulse  did  not  give  to  the 
finger  the  impression  of  its  being  a  high  tension  pulse. 

It  was  described  as  being  a  pulse  of  very  small  volume, 
moderately  well  sustained,  and  subsiding  under  the  finger 
between  the  beats  about  as  rapidly  as  normal.  i 

The  nutrition  of  the  left  ventricle  must  have  been  fairly 
good  for  it  to  maintain  such  a  blood  pressm-e.  The  smallness 
of  the  volume  was  doubtless  due  to  the  deficiency  in  the  amount 
of  blood  which  the  right  ventricle  was  able  to  keep  in  circula- 
tion, and  in  this  connection  the  questions  arise,  How  far  was 
the  high  blood  pressure  due  to  some  pathological  change  in 
the  condition  of  the  arterioles,  the  result  of  the  kidney  disease  ?  ; 
and.  How  far  was  it  a  compensatory  phenomena  necessitated 
by  the  small  volume  of  blood  which  was  available  for  the  left 
ventricle  ?  | 

The  fact  that  the  apex  was  about  one  inch  outside  the     / 
nipple  hne  and  in  the  fifth  space  might  be  taken  as  suggesting    | 
that  there  had  been  in  the  past  dilatation  due  to  the  over-    \ 
action  necessitated   by   arterial   contraction   such   as  results    1 
from  kidney  disease.  \ 

The  presence  of  some  dilatation  of  the  left  ventricle  supports  \ 
the  evidence  given  by  the  right  ventricle  as  to  the  absence 
of  any  marked  degree  of  rigidity  of  the  heart  wall.  It  is  / 
probable  that  the  possession  of  an  unusual  degree  of 
distensibiUty  accounted  for  the  unusual  featm-es  of  this  case. 
For  it  is  not  common  to  find  a  man  able  to  continue  working, 
as  he  did,  in  spite  of  such  a  great  amount  of  breathlessness. 
It  is,  I  think,  fair  to  assume  that  if  the  right  ventricle  had 
been  more  rigid  than  it  was,  it  would  not  have  been  able  to 
adapt  itself  to  the  altered  conditions  of  the  circulation,  and 


160  LATER  LIFE 

that,  under  such  circumstances,  the  man's  condition  would 
have  been  much  less  satisfactory  than  it  actually  was. 

And  now  we  had  better  conclude  this  essay  by 
summarising  the  various  points  which  are  apt  to  give  rise  to 
difficulty  in  the  diagnosis  of  heart  failure  in  later  life. 

Li  the  first  place,  we  must  mention  the  main  cause — namely, 
that  the  ordinary  and  easily  recognised  form  of  failure  with 
enlargement  of  the  heart  does  not  constitute  anything  Hke 
so  large  a  proportion  of  all  cases  as  it  does  earlier  in  life. 
In  other  words,  we  more  often  meet  in  later  life  cases  where 
failure  is  unaccompanied  by  enlargement  and  evidence  of 
venous  plethora,  and  therefore  we  have  more  cases  where 
the  signs  of  failm-e  are  few  and  require  careful  observation 
to  recognise  them. 

Again,  another  set  of  difficulties  arises  from  the  tendency 
of  the  heart  to  partake  in  the  general  increase  in  stiffness  (or 
rigidity)  which  is  apt  to  characterise  other  tissues  of  the  body 
as  age  advances.  This  also  tends  to  lessen  the  likelihood  of 
obvious  signs  of  heart  failure  being  found,  whether  they  be 
of  the  nature  of  enlargement  or  of  diminution  in  its  size  as 
clinically  recognised. 

Another  set  of  difficulties  arises  owing  to  the  changes  that 
are  apt  to  take  place  in  the  arteries  in  later  life  and  the  frequency 
with  which  high  blood  pressure  and  arterial  disease  occurs, 
rendering  the  pulse,  very  often,  quite  an  uncertain  guide,  and 
because  an  apparently  strong  pulse  may  really  be  a  dangerously 
weak  high-pressure  one. 

Arterial  disease  is  also  accountable  for  another  set  of 
diagnostic  difficulties  that  we  have  to  face — namely,  those 
due  to  the  fact  that  in  later  life  a  common  cause  of  heart 
failure  is  the  gradual  interference  with  its  nutrition,  which 
disease  of  the  coronary  arteries  induces,  and  the  fact  that 
such  interference  is  usually  greater  on  one  side  of  the  heart 
than  the  other.  We  therefore  have  to  be  prepared  to  meet 
with  cases  whose  one  ventricle  is  strong  and  the  other  one 
is  weak. 

This  same  onset  of  malnutrition  in  later  life  may  be  difficult 
to  recognise  in  hearts  that  are  already  enlarged  as  the  result 
of  valvular  disease  or  of  overstrain  occm-ring  earlier  in  life. 


DIAGNOSTIC  DIFFICULTIES  161 

Here,  again,  the  '  negative  '  signs  (using  the  word  in  its  mathe- 
matical sense)  of  myocardial  failure  interacting  upon  the 
positive  ones  of  the  pre-existing  heart  failure  will  not  give  very 
easily  recognised  evidence  of  their  presence. 

A  very  large  number  of  difficulties,  in  such  cases  as  we  are 
speaking  of,  depend  upon  the  fact  that  a  weak  heart  circulates 
less  blood  than  normal,  and  that,  as  a  result,  the  venous  cii'cula- 
tion  is  lessened  in  volume,  in  contrast  to  failure  in  a  strong 
heart,  where  the  volume  of  blood  in  the  veins — and  especially 
the  thoracic  ones — is  increased. 

We  may  therefore  meet  with  a  large  number  of  apparently 
contradictory  evidences  of  heart  failure  and  physical  signs 
— such  as  increased  fullness  of  the  veins,  diminution  in  the 
size  of  the  right  ventricle,  &c. — which  may  show  either  improve- 
ment or  deterioration  in  the  condition  of  the  heart,  according  to 
the  circumstances  under  which  they  occm-.  These  paradoxes 
appear  worse  on  paper  than  they  prove  at  the  bedside ;  but 
it  is  necessary  to  be  on  the  alert  for  their  occurrence.  Here 
is  a  list  of  some  of  them  : — 

Increased  fullness  of  the  veins  in  a  moderately  weak  heart 
means  deterioration,  and  in  a  very  weak  one  means  improve- 
ment ;  and,  conversely,  lessened  fullness  means  improvement 
in  a  heart  only  moderately  weak,  and  deterioration  in  a  very 
weak  one. 

Extreme  emptiness  of  the  veins  of  the  neck  is  a  very  good 
sign  in  a  moderately  weak  heart,  and  a  dangerously  bad  sign 
in  a  very  weak  one. 

As  regards  the  heart  :  dilatation  of  the  right  or  left 
ventricle  in  a  moderately  weak  heart  is  the  commonest  sign 
of  heart  failure,  but  in  a  case  of  severe  myocardial  weakness 
dilatation  is  the  usual  sign  of  returning  strength.  Again,  the 
lessening  in  the  size  of  a  slightly  dilated  ventricle  in  a  moderately 
weak  heart  would  be  a  sign  of  improvement,  but  in  a  very 
weak  one  it  would  probably  mean  dangerous  muscular  failure. 

Absence  of  dilatation  in  pneumonia  would  be  a  good  sign 
if  the  heart  were  strong ;  but  it  may  also  {vide  p.  97)  be  a 
sign  of  very  dangerous  myocardial  weakness. 

The  same  rule  holds  with  regard  to  the  heart  sounds  ;  for, 
where  they  are  unduly  loud — say,  those  of  the  right  ventricle 


162  LATER  LIFE 

when  the  left  is  failing — a  lessening  in  their  loudness  may  be 
due  to  the  recovery  of  the  left  side,  or  to  the  onset  of  muscular 
weakness  on  the  right  side,  as  the  result  of  the  overstrain — a 
very  alarmmg  condition. 

There  are  also  some  points  with  regard  to  the  Uver  ;  for, 
while  a  diminution  in  the  size  of  a  liver  which  is  enlarged 
by  tricuspid  regurgitation  is  usually  a  good  sign,  a  sudden 
lessening  of  its  size  might  be  a  sign  of  the  onset  of  myocardial 
weakness,,  as  in  the  case  mentioned  at  p.  63, 

Also  in  this  comiection  the  fact  must  be  remembered 
that  a  tense  liver  may  give  a  resonant  note  by  conduction 
of  vibrations  to  and  from  an  air  containing  viscus  below  it, 
whereas  when  less  distended  with  blood  it  does  not  do  so. 
Therefore,  as  a  case  of  tricuspid  regm-gitation  with  an  enlarged 
liver  improves,  the  area  of  absolute  Uver  dullness  in  the  epigas- 
trium may  sometimes  be  found  to  increase  downwards,  and 
the  incautious  observer  may  fear  that  the  patient  is  getting 
worse.  This  mistake  can  easily  be  prevented  by  noting  the 
level  at  which  the  liver  edge  can  be  felt,  it  will  be  found  in 
such  a  case  to  rise  as  the  level  of  the  absolute  dullness 
descends. 


Essay  II.— ON  THE  VALUE  OP  AN  ABNORMAL  RISE 
IN  THE  AVERAGE  LEVEL  OF  THE  DIAPHRAGM 
AS  A  GUIDE  TO  THE  VOLUME  OF  BLOOD  IN 
ACTIVE    CIRCULATION  ^ 

The  object  of  this  essay  is  to  bring  forward  clinical  evidence  in 
favour  of  the  following  propositions  : — 

1.  When,  from  any  cause,  the  total  volume  of  the  blood 
in  circulation  is  materially  diminished,  the  total  bulk  of  the 
intrathoracic  viscera  is  correspondingly  diminished  by  the 
relative  emptiness  of  the  thoracic  blood-vessels,  especially 
those  of  the  lungs.  This  diminution  in  the  bulk  of  the  intra- 
thoracic contents  shows  itself  by  an  elevation  of  the  diaphragm, 
which  has  to  be  maintained  at  a  higher  average  level  than  the 
normal  in  order  to  adjust  the  cubic  content  of  the  thorax 
to  the  altered  volume  of  its  contained  viscera. 

2.  That  such  a  rise  of  the  diaphragm  may  frequently  be 
detected  clinically,  and,  when  present,  is  of  value  in  diagnosis 
and  affords  important  indications  for  treatment. 

Normal  Position  of  the  Diaphragm 

The  position  of  the  diaphragm  can  be  recognised  clinically 
by  ascertaining  the  upper  level  of  the  gastric  resonance  in  the 
left  nipple  line,  or  of  the  upper  border  of  the  liver  in  the  right 
nipple  Hne.  In  both  cases  percussion  is  best  done  with  the 
patient  recumbent ;  and  in  the  case  of  the  gastric  resonance 
the  recumbent  posture  is  essential  to  accuracy,  because  in 
the  erect  posture  the  gaseous  contents  of  the  stomach,  if 
scanty,  may  rise  up  into  the  arch  of  the  diaphragm,  and  the 
duUness  of  the  liquid  contents  of  the  stomach  be  continuous 
with  the  duUness  of  the  left  lobe  of  the  hver  and  the  heart. 

'  Read  before  the  Birmingham  Branch  of  the  British  Medical  Association. 
See  the  British  Medical  Journal,  April  27,  1907. 

163  m2 


164  HIGH  DIAPHKAGM  A  SIGN  OF 

Of  the  two  methods  named,  the  percussion  of  the  gastric 
resonance  is  easier  and  more  rehable  for  the  following  reasons  : — 

1.  There  is  much  variation  in  the  upper  level  of  the  liver 
dullness  of  healthy  individuals,  dependent  upon  the  degree  to 
which  the  lungs  have  been  expanded  by  exercise  or  athletics,  &c. 

2.  The  respiratory  movements  of  the  lower  edge  of  the 
lung  render  exact  accuracy  of  record  as  to  its  level  impossible. 

3.  The  level  of  the  diaphragm  on  the  right  side  is  more  apt 
to  be  interfered  with  by  ill- defined  pathological  conditions  of 
the  lung  than  is  the  case  with  the  level  of  the  central  tendon 
which  underlies  the  heart. 

Gastric  Eesonance 

For  the  study  of  the  gastric  resonance  it  is  necessary,  as 
before  mentioned,  for  the  subject  to  be  lying  on  his  back,  so 
that  any  gas  in  the  stomach  may  come  to  the  front  and  give 
a  contrast  with  the  dullness  of  the  left  lobe  of  the  liver  and 
the  heart,  which  lie  above  it. 

The  determination  of  the  area  over  which  the  gastric 
resonance  is  obtainable  is  sometimes  rendered  more  easy  by 
listening  to  the  area  over  which  *  reverberation  '  can  be  heard 
when  some  continuous  sound  is  communicated  to  the  air  in 
the  stomach.  This  is  simply  done  by  means  of  a  short  rough 
rod,  which  is  pressed  over  the  stomach  area  and  scratched 
regularly  with  the  fingernail.  The  echo,  similar  to  the  bell 
sound  in  pneumothorax,  is  clearly  heard  over  the  whole  gastric 
area,  but  is  sharply  limited  to  it  {vide  Essay  XVI,  p.  480). 

As  a  rule  the  results  obtained  by  percussion  and  by  noting 
the  area  of  gastric  reverberation  coincide  very  closely  with 
each  other. 

By  these  methods  the  normal  level  of  the  upper  limit  of 
the  gastric  resonance  is  found  to  be  in  the  sixth  left  interspace. 
It  sometimes  in  health  reaches  the  upper  border  of  the  sixth 
rib,  but,  as  a  rule,  when  it  reaches  the  fifth  interspace  it  must  be 
considered  pathological.  Only  once  or  twice  have  I  found  well- 
marked  gastric  resonance  in  the  fifth  interspace  in  a  person  who 
was  apparently  in  perfect  health,  and  under  ckcumstances  which 
pointed  to  its  being  the  normal  level  for  the  individual  concerned. 


DIMINISHED  BLOOD  VOLUME  165 

Upper  Level  of  the  Liver  Dullness 

Although  the  percussion  of  the  upper  border  of  the  liver 
is  of  less  value  than  that  of  the  stomach,  where  exact  observa- 
tions are  desired  upon  the  level  of  the  diaphragm,  it  neverthe- 
less gives  us  important  information  as  to  the  condition  of 
the  diaphragm,  for  its  elevation  above  the  normal  level 
may  be  very  great  when  the  diaphragm  is  high.  Thus  in  one 
patient  (Case  XI)  there  was  distinct  relative  Hver  dullness  up  to 
the  middle  of  the  third  rib  in  the  right  nipple  line. 

The  percussion  of  the  upper  border  of  the  liver  dullness  is 
also  of  considerable  value,  because  it  often  gives  an  indication 
as  to  the  amount  of  arching  of  the  diaphragm  present,  if  the 
distance  between  the  level  of  the  absolute  dullness  and  that 
of  the  relative  Hver  dullness  be  carefully  observed,  and  the 
changes  dming  respiration  noted.  Thus  a  wide  area  of 
relative  dullness  suggests  an  abnormally  arched  diaphragm 
and  a  sudden  change  from  full  lung  resonance  to  absolute 
liver  dullness  suggests  a  flatter  diaphragm,  as  in  emphysema. 

This  abnormal  wideness  of  the  area  of  relative  dullness, 
indicating  a  highly  arched  diaphragm,  is  well  shown  in  some 
of  the  following  diagrams — namely,  figs.  10,  19,  27,  31,  41. 

Observation  of  the  Lower  Edge  of  the  Liver 

The  careful  mapping  out  of  the  lower  edge  of  the  liver  dullness 
is  also  of  importance  in  the  study  of  the  level  of  the  diaphragm, 
because  as  the  diaphragm  rises,  the  rise  of  the  lower  border 
of  the  liver  dullness  is  often  more  marked  than  the  upper. 
It  is  not  uncommon  to  find  in  such  cases  a  total  disappearance 
of  the  absolute  dullness  of  the  hver,  internal  to  the  right  nipple 
line,  accompanied  by  a  marked  rise  in  the  lower  edge  of  the 
liver,  sometimes  to  the  extent  of  2  inches  or  more  above  the 
costal  arch.  This  change  is  well  shown  in  figs.  26,  31,  38,  40. 
It  seems  as  if  the  hver  shps  back  into  the  hollow  of  the  diaphragm, 
and  its  lower  anterior  edge  is  thus  drawn  up  and  back  so  much 
that  it  barely  comes  in  contact  with  the  ribs  anteriorly  at  all ; 
and  the  intestinal  or  gastric  resonance  meets  the  lung  resonance 
over  this  area.     This  strange  change  in  the  shape  of  the  absolute 


166 


HIGH  DIAPHRAGM  A  SIGN  OF 


dullness  of  the  liver  will  sometimes  develop  in  a  week  or  so,  and 
then  as  speedily  give  way  to  the  normal  relationship  of  the 
liver  dullness  to  the  costal  arch,  when  the  conditions  causing 
the  ascent  of  the  diaphragm  subside  (Case  IV).  (See  also 
pp.  187, 188.) 


Scope  of  Subject 

Though  this  essay  does  not  deal  with  cases  in  which  the 
level  of  the  diaphragm  is  altered  by  some  obvious  physical 

Cases    showing  Elevation  of  the  Diaphragm  from  Collapse  of  the 

Left  Lung 


ormal 
level 


To  mid 
axilla 


ormaJ, 
level 


Fig.  22. — Case  I  :  Normal  Chest. 


Fig.  23. — Case  II :    Collapse 
OF  Lung. 

Diaphragm  high  on  left  side  only. 


cause — such  as  the  pressure  of  distended  abdominal  viscera, 
or  the  traction  of  a  collapsed  or  fibrosed  lung — nevertheless, 
it  may  be  well  to  say  a  few  words  as  to  the  changes  which  take 
place  when  the  left  lung  shrinks  from  healing  tuberculosis,  or 
remains  unexpanded  after  compression  by  extensive  pleurisy. 
In  these  cases  we  know  that  the  diaphragm  is  drawn  up  by 
the  lessened  size  of  the  left  lung,  and  as  the  changes  which  take 
place  in  the  level  of  the  gastric  resonance  are  precisely  those 
which  occur  in  the  cases  dealt  with  in  this  paper  this  may  be 
taken  as  evidence  in  favour  of  the  points  raised. 

I  give  the  notes  and  figures  of  two  such  cases,  one  moderate 
and  one  extreme. 


DIMINISHED  BLOOD  VOLUME 


167 


Case  IL — Moderate  Elevation 

The  heart  is  drawn  up  a  httle  to  the  left  by  the  rise  of  the 
diaphragm,  but  there  is  a  marked  rise  in  the  gastric  resonance 
{vide  fig.  23)  not  only  in  the  left  nipple  hne,  but  much  more 
so  in  the  axilla.  Instead  of  there  being  no  gastric  resonance  in 
the  axilla,  as  in  the  normal  chest,  in  this  case  the  resonance 
reached  the  fourth  interspace  in  the  nipple  line  and  extended 
nearly  to  the  anterior  axillary  hne,  4  inches  from  the  sternum. 
In  the  fifth  space  it  reached  5i  inches,  and  in  the  sixth 
space  there  was  full  gastric  resonance  and  reverberation  to  the 
mid-axillary  hne,  6|  inches 
from  the  sternum ;  the 
lower  border  was  at  the 
eighth  rib. 

This  condition  developed 
on  the  rapid  absorption  of  _       „ 

pleuritic  effusion,  and  in  [  \\f(^p^7r-^  ^^^J\iV  \Topqst 
eleven  days  the  upper 
border  of  the  gastric  reson- 
ance had  returned  to  the 
normal  level,  and  there  was 
none  in,  or  external  to,  the 
anterior  axillary  line. 


Case  III. — Extreme 
Elevation 


miliary 
line 


^rm&l 


-Case  III :   Collapse  of 
Lxma. 

Very  high  left  diaphragm. 


There  was  complete  non- 
expansion  of  the  left  lung 
(fig.  24).     The  right  lung 

crossed  over,  and  its  left  border  could  be  detected  just  internal  to 
the  left  nipple  hne  (2^  inches  from  the  sternal  edge)  on  expiration, 
and  during  full  inspiration  it  crossed  to  beyond  the  nipple  hne 
(more  than  4  inches  from  the  left  edge  of  the  sternum)  in  the 
second,  third,  and  fourth  interspaces.  This  shows  the  extreme 
shrinkage  of  the  left  lung.  The  diaphragm  also  was  correspond- 
ingly high,  as  judged  by  the  level  of  the  gastric  resonance. 

The  expansion  of  the  right  lung  pushing  down  the  heart 
prevented  any  great  rise  of  the  diaphragm  in  the  nipple  line, 
and  it  was  only  at  the  fifth  interspace  ;  but  in  the  axilla  there 
was  full  gastric  resonance  to  the  posterior  axillary  line  in  the 
sixth  space,  8  inches  from  the  middle  line.  Its  lower  border 
was  in  the  eighth  space. 


168     '  HIGH  DIAPHRAGM  A  SIGN  OF 

High  Diaphragm  in  Enteric  Fever 

Although,  in  common  with  all  those  who  carefully  percuss 
the  cardiac  dullness,  I  have  long  been  conscious  that  there 
is  occasionally  abnormal  resonance  below  the  cardiac  area,  I 
did  not  give  the  subject  special  attention  till  the  following 
case  brought  it  forcibly  under  my  notice  : — 

A  man  suffering  from  an  extremely  severe  attack  of  enteric 
fever  presented  very  great  asthenia,  but  no  complications  of 
any  sort  until  the  end  of  the  third  week.  He  then  became 
decidedly  feebler,  although  the  temperature  was  not  specially 
high,  and  the  condition  of  the  abdomen  was  satisfactory.  He 
had  had  no  diarrhoea.  This  asthenia  was  suggestive  of  the 
virulence  of  the  poison  he  was  absorbing  ;  but  as  his  condition 
became  worse  it  was  evident  that  some  other  cause  was  at  work. 

The  abdomen  from  being  moderately  full  became  abnormally 
retracted,  and  his  face  and  limbs  gave  the  appearance  of 
extreme  emaciation.  This  rapid  change  in  his  appearance  was 
evidently  due  to  lack  of  liquids  in  the  body.  He  was  taking 
three  pints  of  milk  daily,  besides  some  water.  I  tried  the  effect 
of  a  subcutaneous  saline  injection  of  half  a  pint  or  more  ;  it 
was  rapidly  absorbed,  but  as  rapidly  excreted  by  the  kidneys, 
and  the  patient's  condition  was  in  no  way  improved.  There 
was  a  peculiar  expiratory  type  of  dyspnoea,  which  I  have  now 
learned  to  associate  with  this  condition,  and  also  a  decided 
elevation  of  the  diaphragm,  the  gastric  resonance  reaching 
well  into  the  fifth  space,  and  the  hver  being  decidedly  above 
its  usual  level  in  the  right  nipple  line.  He  died  within  two  or 
three  days  of  these  symptoms  becoming  noticeable. 

Post-mortem,  the  diaphragm  was  at  the  third  rib  on  the  left 
and  at  the  fourth  rib  on  the  right  side  ;  the  heart  was  small, 
its  lower  border  at  the  fourth  interspace,  and  all  the  organs 
dry  and  bloodless. 

In  thinking  over  the  cause  of  death,  I  was  forced  to  the 
conclusion  that  death  was  practically  due  to  starvation,  owing 
to  the  interference  with  intestinal  absorption,  which  resulted 
from  inflammatory  changes  in  the  mesenteric  lymphatics,  and 
my  explanation  of  the  case  was  as  follows  ; — 

t       This  defective  absorption  from  the  intestines,  coupled  with 
the  tissue-waste  due  to  the  fever,  would  presumably  in  course 


DIMINISHED  BLOOD  VOLUME  169 

of  time  lessen  the  proteids  in  the  body  to  such  a  degree  that  the 
total  volume  of  the  blood  would  have  to  diminish  in  order  to 
prevent  it  from  becoming  too  dilute.  This  diminution  at  last 
became  so  extreme  that  the  proper  nutrition  of  brain  and 
heart  was  no  longer  possible,  and  the  patient  died.  The 
explanation  of  the  elevation  of  the  diaphragm  which  appeared 
to  be  most  probable  was  that  the  diminution  in  volume  of  the 
circulating  blood  caused  such  a  lessening  in  the  size  of  the  heart 
and  such  emptiness  of  the  pulmonary  artery  and  great  vessels 
that  the  volume  of  the  heart  and  lungs  was  so  materially 
diminished  that  the  diaphragm  had  to  rise  so  as  to  diminish 
the  cubic  content  of  the  thorax  to  a  corresponding  extent. 

I  have  had  some  confirmation  of  this  explanation  of  the 
preceding  case,  for  I  have  on  several  occasions  seen  the  same 
symptoms  appearing  in  severe  cases  of  enteric  fever.  When  I 
have  detected  the  pecuhar  sighing  breathing  and  the  elevation 
of  the  diaphragm,  associated  with  signs  of  lack  of  fluid  in  the 
body,  I  have  been  able  at  once  to  remove  the  dangerous 
pymptoms  by  the  administration  of  peptones  and  of  milk 
sugar,^  the  absorption  of  which  takes  place  through  the  portal 
vein  and  not  through  the  intestinal  lymphatics. 

It  is  now  some  years  since  I  have  seen  such  a  case,  because 
I  am  careful  to  guard  against  such  malnutrition. 

High  Diaphragm  in  Limitation  of  Food 

If  the  above  suggestion  were  accurate  and  a  limitation  of 
the  intake  of  nutritive  material  would  (if  carried  to  excess) 
cause  a  diminution  in  the  total  volume  of  the  blood,  and  show 
itself  by  a  shrinking  of  the  thoracic  contents,  the  same  phe- 
nomenon of  high  diaphragm  ought  to  be  found  where  semi- 
starvation  is  adopted  as  a  therapeutic  measure — for  instance, 
in  the  treatment  of  gastric  ulcer. 

For  many  years  I  have  noticed  that  as  a  rule  in  cases  of 
gastric  ulcer  there  is  a  marked  rise  in  the  diaphragm  after  some 

'  The  administration  of  sugar  in  enteric  fever  must  only  be  resorted  to 
in  such  cases  as  these.  In  ordinary  cases  it  appears  greatly  to]  increase  the 
severity  of  the  syinptoms — presumably,  by  feeding  the  baciUi  more  than  it 
feeds  the  patient. 


Case  of  Gastric  Ulcee,  showing  a  High  Diaphragm  due  to  Starvation 


Fig.  25. — Case  IV  :    Gastric 
Ulcer. 

March  7.    Before  limitation  of  food. 


Fig.  26.— Case  IV. 

March  13.    After  six  days  of  rectal 
feeding. 


'omml 
level 


Fig.  27.— Case  IV. 

March  15.     More  food  given  ;  heart  larger. 


>rmAl 


Fig.  28.— Case  IV. 
March  19.    Food  increased. 


DIMINISHED  BLOOD  VOLUME 


171 


days  of  strict  limitation  of  food,  as  where  the  patient  is  fed 
only  by  nutrient  enemata. 

The  amount  and  the  duration  of  the  rise  varies  much  in 
different  cases.  In  some  the  gastric  resonance  will,  after  a 
a  few  days  of  rectal  feeding,  rise  into  the  fifth  interspace,  or 
even  into  the  fourth,  and  as  rapidly  return  to  the  normal  level 
on  the  resumption  of  full  feeding.  In  others  the  rise  may  take 
place  more  slowly,  attaining  its  maximum  height  after  the 


^rmal 


Fio.  29.— Case  IV. 

Marcli  29.    Tran  sient  cardiac  dilatation. 


Fig.  30.— Case  IV. 

March  30.    Practically  normal. 


cessation  of  rectal  feeding,  and  only  returning  to  the  normal 
level  after  the  patient  has  been  on  ordinary  diet  for  some  time. 
The  following  case  shows  an  unusually  rapid  rise  and  fall 
of  the  diaphragm,  and  is  illustrated  by  figs.  25-30  and  by  a 
table  showing  the  details  as  to  the  rise  and  fall  of  the  diaphragm. 


CASES    OF    GASTKIC    ULCEE 

Case  IV. — Gastric  Ulcer 

Kate  G.,  aged  thirty-eight,  admitted  to  hospital  March  6, 
1906  (figs.  25-30).  There  was  a  history  of  dyspepsia  of  many 
years'  standing,  and  an  attack  of  haematemesis  six  years  ago. 
Present  illness  dates  back  to  an  attack  of  influenza  three  weeks 
ago  ;  ten  days  ago,  an  attack  of  vomiting  was  followed  four  days 
later  by  haematemesis,  half  a  pint  of  blood  being  brought  up. 


172 


HIGH  DIAPHRAGM  A  SIGN  OF 


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DIMINISHED  BLOOD  VOLUME  173 

On  admission,  much  pallor.  Pain  after  food,  and  epigastric 
tenderness  were  noted.  Examination  of  the  abdomen  showed 
that  the  diaphragm  was  rather  high,  the  gastric  resonance 
reaching  up  to  the  upper  border  of  the  sixth  rib,  and  the  lower 
border  of  the  hver  being  1|  inches  above  the  costal  arch.  There 
was  1^  inches  of  relative  liver  dullness  in  the  right  nipple  line. 
She  was  fed  entirely  by  the  rectum  for  a  week,  and  then  the  food 
was  gradually  increased. 

The  rise  of  the  diaphragm,  and  its  return  to  normal,  are  well 
shown  in  figs.  25,  26,  27,  28,  29,  and  30,  and  also  in  the  table 
given.  With  regard  to  fig.  29,  the  transient  dilatation  upwards 
of  the  heart  is  of  the  type  usually  seen  in  ansDmia. 

The  following  is  such  a  case  : — 

Case  V. — Gastric  Ulcer  with  Severe  loss  of  Blood 

Nelly  Y.,  aged  twenty,  admitted  January  18,  was  kept  on 
nutrient  enemata  only  till  January  20,  then  allowed  one  pint 
of  milk  a  day  as  well.  This  diet  was  increased  gradually 
till  by  February  10  she  was  taking  a  full  fish  diet. 

The  stomach  resonance  and  the  liver  dullness  (figs.  31-33) 
continued  to  rise  till  January  29,  when  they  stood  at  the 
upper  border  of  the  fifth  left  and  fourth  right  ribs  respectively. 
At  this  date  she  had  been  for  two  days  on  an  ordinary  bread- 
and-milk  diet.  By  February  10  there  was  still  some  eleva- 
tion of  the  diaphragm,  but  the  relationships  of  the  organs  were 
more  normal. 

High  Diaphragm  after  Severe  Hemorrhage 

Closely  allied  to  these  cases  are  those  where,  after  a  sudden 
severe  haemorrhage,  the  diaphragm  may  be  found  to  be  an 
interspace  or  more  above  the  normal  level. 

High  diaphragm,  if  looked  for,  can  very  often  be  found  in 
such  cases  as  are  blanched  by  severe  haemorrhage,  and  the 
gradual  return  of  the  diaphragm  to  the  normal  level  can  be 
observed  as  the  patient  recovers  (fig.  84). 

Case  VI. — Hematemesis 

Louisa  C,  aged  thirty-three,  admitted  with  very  severe 
hsematemesis.  She  was  so  blanched  that  the  foot  of  her  bed 
had  to  be  kept  elevated  to  prevent  faintness. 


A  Case  of  Gastric  Ulcbb  Showing  a  High  Diaphragm 


mid 
^axilla 


ormaJ 


Fig.  31. — Case  V  :    Gastric 
Ulcer. 

January  20.    After  three  days  of  rectal 
feeding. 


Fig.  32.— Case  V. 

January  29.    More  food  ;  diaphragm 
lower. 


hrmaJ 
level 


High  Diaphragm  the  Result 

OF  HiEMORRHAGE 


ormal 


Fig.  33.— Case  V. 

Diaphragm  lower. 


FiQ.  34. — Case  VI :   Hjematemesis. 


High  Diaphbaqm  in  Anaemia 


ormal 


Fia.  35.— Case  VII :   An-simia. 
Eigh  diaphragm  and  dilated  heart. 


tomid 


hrmal 


Fia.  36. — Case  VIII :  Ak^emia  . 

February  15.    Diaphragm  very  high  ia 
axilla. 


High  Diaphragm  in  Myxcedema 


Fig.  37.— Case  VIII. 

March  29.    Nearly  normal. 


Fig.  38.— Case  IX. 

Neurasthenia. 


176  HIGH  DIAPHEAGM  A  SIGN  OF 

The  figure  (34)  shows  the  marked  rise  in  the  level  of  the 
gastric  resonance,  and  of  the  lower  edge  of  the  Hver  ;  also  the 
broadening  of  the  relative  liver  dullness.  In  this  case  there 
was  full  intestinal  resonance  for  2  inches  above  the  costal  arch 
in  the  right  nipple  hne. 

High  Diaphragm  in  Anemia 

In  anaemia,  from  causes  other  than  loss  of  blood,  the  same 
phenomenon  of  high  diaphragm,  though  by  no  means  constant, 
is  very  frequently  noticed.  In  a  series  of  consecutive  obser- 
vations upon  cases  of  anaemia  and  chlorosis  I  found  a  well- 
marked  rise  of  the  diaphragm — that  is,  to  the  fifth  interspace, 
or  higher — in  about  one-third  of  the  cases  ;  but  I  was  not 
able  to  determine  the  exact  reason  for  the  difference  in 
this  respect  without  a  fuller  investigation  into  the  blood 
changes  present  in  each  case  than  the  time  at  my  disposal 
permitted. 

In  true  chlorosis  it  has  been  stated  that  the  volume  of  the 
blood  is,  if  anything,  increased  ;  and  if  this  be  proved  to  be  so, 
the  observation  of  the  level  of  the  diaphragm  may  prove  of 
diagnostic  value  in  these  cases. 

The  reason  for  the  rise  of  the  diaphragm  in  anaemia  can- 
not be  definitely  stated.  It  may  be  the  result  of  deficiency 
of  proteids,  or  it  may  be  due  to  deficiency  of  iron  or  some  other 
necessary  constituent  of  the  blood,  acting  in  the  same  way  as 
the  deficiency  of  food  acts. 

This  hypothesis  may  be  expressed  in  general  terms  by 
saying  that  the  total  volume  of  the  blood  diminishes  because 
there  is  a  deficiency  of  some  one  or  more  of  the  essential  con- 
stituents of  the  blood,  and  therefore  the  total  volume  of  the 
blood  in  circulation  must  be  lessened  in  order  to  keep  the 
percentage  of  that  substance  at  its  irreducible  minimum. 

In  these  cases  of  anaemia  the  area  of  cardiac  dullness  is, 
as  a  rule,  larger  than  in  the  cases  previously  mentioned.  This 
is  due  to  the  frequent  presence  of  dilatation  of  the  right  ventricle. 

In  connection  with  these  changes  in  anaemia  there  is  one 
result  of  high  diaphragm  which  may  have  been  misinterpreted 
in  the  past — namely,  the  displacement  upwards  of  the  apex 
beat.     In  papers  I  have  written  and  seen  upon  this  subject 


DIMINISHED  BLOOD  VOLUME  177 

this  upward  and  outward  displacement  of  the  apex  of  the 
heart  in  anaemia  has  been  explained  solely  by  changes  in  the 
heart  itself.  I  am  now  sure  that  in  some  of  the  cases,  at  all 
events,  the  rise  in  the  diaphragm  must  play  some  part  in  the 
upward  displacement. 

Case  VII. — Severe  Anjemia. 

Cissy  G.,  aged  thirty-one.  The  gastric  resonance  reached  well 
into  the  fourth  left  interspace,  and  in  the  fifth  interspace  there 
was  well-marked  gastric  resonance  throughout  the  whole  inter- 
space from  the  sternum  to  the  anterior  axillary  line  (fig.  35). 
The  heart  was  displaced  upwards,  and,  owing  to  the  anaemic 
dilatation  of  the  right  ventricle,  there  was  a  larger  area  of  dull- 
ness than  in  the  cases  of  gastric  ulcer  without  marked  anaemia. 
There  was  some  cardiac  impulse  in  the  fourth  interspace,  but 
the  maximum  impulse  was  in  the  third  left  interspace  external 
to  the  nipple  fine  (3  inches  from  the  sternum).  In  the  second 
left  interspace  there  was  relative  dullness  and  pulsation  for 
2  inches  from  the  sternum. 

Case  VIII. — Anemia 

Ada  F.,  aged  seventeen.  Admitted  to  hospital  February  15, 
with  anaemia  and  severe  chilblains.  On  admission  the  area  of 
cardiac  dullness  was  smaU,  there  being  no  absolute  dullness, 
and  the  gastric  resonance  was  very  high — namely,  up  to  the 
middle  of  the  fom'th  rib  in  the  left  nipple  line.  There  was 
also  a  great  increase  towards  the  axilla,  for  gastric  resonance 
and  reverberation  were  clearly  obtainable  in  the  fourth  inter- 
space near  to  the  mid-axiUary  line  (fig.  36).  In  the  course  of 
ten  days  the  diaphragm  was  lower,  the  gastric  resonance  reach- 
ing only  to  the  fifth  rib,  and  only  extending  into  the  axilla  in 
the  sixth  and  seventh  interspaces.  After  being  in  hospital  six 
weeks  the  stomach,  though  still  up  to  the  fifth  rib,  did  not 
reach  into  the  axilla  at  all,  and  the  cardiac  dullness  was  larger, 
showing  some  anaemic  dilatation. 

High  Diaphragm  in  Neurasthenia 

Li  many  other  diseases  a  high  diaphragm  may  occasionally 
be  met  with  ;  but  in  cases  of  neurasthenia  it  is  of  such  relatively 
frequent  occurrence  as  to  raise  the  question  whether  in  this 
condition  some  of  the  chemical  or  organic  constituents  of  the 
blood  are  not  deficient  in  amount. 


178  HIGH  DIAPHRAGM  A  SIGN  OF 

Case  IX. — Neurasthenia 

A  case  of  a  somewhat  similar  nature  is  that  of  a  labouring 
man  who  was  sent  to  me  as  a  possible  mahngerer,  because  he 
looked  comparatively  hale  and  hearty,  but  nevertheless  com- 
plained of  great  lassitude  and  inabihty  to  work.  His  colour 
was  good  ;  there  was  no  complaint  except  of  a  little  atonic 
dyspepsia.  Physical  examination  showed  nothing  except  a 
high  diaphragm,  the  gastric  resonance  reaching  to  the  fourth 
left  interspace  and  the  absolute  dullness  of  the  liver  being 
absent  internal  to  the  right  nipple  line  (see  fig.  38).  There 
were  some  symptoms  which  suggested  the  possibihty  of 
deficiency  of  thyroid  secretion,  and  treatment  by  thyroid 
extract  entirely  cured  him. 

Commentary 

"We  must  now  discuss  the  explanation  of  the  phenomena 
described  and  illustrated  by  the  diagrams  given. 

Is  it  right  to  conclude  that  elevation  of  the  gastric  resonance 
on  the  left  side  and  of  the  fiver  dullness  on  the  right  side 
implies  certainly  an  elevation  of  the  diaphragm  ?  As  the 
phenomena  described,  though  less  marked,  are  stifi  present 
in  the  erect  as  well  as  in  the  recumbent  attitude,  and  as  the 
rise  in  the  gastric  resonance  can  usually  be  noticed  far  back 
in  the  axilla  as  well  as  in  front,  an  affirmative  answer  must  be 
given.     The  diaphragm  is  high  in  such  cases. 

Granted,  then,  that  the  diaphragm  is  high  in  the  cases  of 
which  we  have  been  speaking,  what  is  the  explanation  of  its 
rise  in  this  marked  manner  ? 

It  must  either  be  drawn  up  by  suction  from  above,  or  pushed 
up  by  pressure  from  below  ;  for  we  know  of  no  power  inherent 
in  itself  whereby  the  diaphragm  could  rise  and  compress  the 
thoracic  viscera. 

But  of  these  two  forces  it  is  easy  to  eliminate  pressure 
from  below  as  a  cause  of  the  elevation  of  the  diaphragm. 
In  all  these  cases  the  abdomen  is  empty  or  normal  in  ap- 
pearance, and  there  is  certainly  no  increase  of  intra-abdominal 
pressure. 

Then,  again,  it  cannot  be  due  to  some  peculiar  action  of 
the  stomach,  because  the  rise  is  bilateral,  involving  the  fiver 


DIMINISHED  BLOOD  VOLUME  179 

as  well  as  the  stomach.  Moreover,  a  glance  at  the  diagrams 
wiU  show  that  the  lower  level  of  the  stomach  is  often  raised 
as  well  as  the  upper  border,  and  I  have  never  in  these 
cases  noticed  any  prominence  of  the  stomach  in  the  epi- 
gastrium, such  as  is  always  noticeable  when  the  stomach 
is  suJQQciently  distended  and  tense  to  exert  pressure  on  the 
thoracic  viscera. 

Moreover,  the  pitch  of  the  reverberation  note  as  heard 
over  the  stomach  is  not  of  the  high  and  varying  character 
noticeable  where  the  organ  is  distended  and  undergoing 
contraction. 

We  must  therefore  conclude  that  the  diaphragm  is  drawn 
up  as  the  result  of  some  change  in  the  intrathoracic  pressure. 

What  intrathoracic  force  can  do  this  ? 

Now,  although  there  is  a  danger  of  error  in  reasoning  when 
a  process  of  exclusion  is  used,  we  may,  I  think,  safely  resort  to 
it  in  this  instance. 

The  thorax  contains  practically  only  four  things  whose 
variation  could  materially  alter  the  volume  of  the  thoracic 
contents  :  the  lung  tissue,  including  the  bronchi ;  the  air 
in  the  lungs  and  bronchi ;  the  heart  and  blood-vessels  ;  and 
the  blood. 

Now,  some  of  these  variable  factors  are  easily  excluded. 
(1)  There  can  be  no  abnormal  suction  exerted  by  the  air  in 
the  lungs,  as  there  is  no  mechanical  interference  mth  the 
entrance  or  exit  of  the  ak  from  the  thorax.  (2)  The  actual 
bulk  of  the  lung  tissue  is  not  changed  ;  the  lungs  in  the  cases 
spoken  of  are  healthy. 

The  agency  causing  elevation  of  the  diaphragm  must, 
therefore,  be  either  a  variation  in  the  cardiac  and  vascular 
tissue,  or  in  the  degree  of  distension  of  the  heart  and  blood- 
vessels in  the  thorax  (including  those  of  the  lungs)  with  blood. 
As  the  cardiac  tissue  is  practically  constant  in  bulk  from  day 
to  day,  the  factor  we  are  searching  for  must  consist  of  a  lessening 
in  the  amount  of  blood  contained  in  the  lungs,  heart,  and 
great  vessels  in  the  thorax. 

When  we  consider  how  large  a  proportion  of  the  lung 
tissue  consists  of  capillary  vessels,  how  much  blood  the  veins 
of  the  thorax  and  the  heart  itself  are  capable  of  holding,  it 

N2 


]80  HIGH  DIAPHRAGM  A  SIGN  OF 

is  clear  that  a  decided  diminution  in  the  volume  of  blood 
circulating  in  the  thorax  might  cause  a  distinct  lessening  in 
the  thoracic  contents,  and  the  space  thus  left  vacant  would 
have  to  be  filled  up  either  by  air  or  by  a  corresponding  lessening 
of  the  cubic  content  of  the  thorax  by  means  of  a  rise  in  the 
level  of  the  diaphragm.  There  is,  therefore,  physiological 
justification  for  the  theory  that  the  rise  in  the  diaphragm  is 
caused  by  a  lessening  in  the  amount  of  blood  in  the  thorax. 

These  theoretical  considerations  are  in  accord  with  the 
facts  of  the  cases  mentioned,  for  in  them  there  were  conditions 
leading  to  malnutrition  of  the  body,  and  presumably  also 
lessened  power  of  regenerating  the  blood. 

One  theoretical  consideration  w^iich  follows  upon  the 
clinicial  facts  here  brought  forward  (if  the  explanation  given 
be  correct)  is  that  there  must  be  a  limit  below  which  the  specific 
gra^dty  of  the  blood  (or  the  percentage  composition  of  its 
various  constituents)  is  not  allowed  to  fall.  Where  there  is 
a  lessened  intake  of  food,  when  the  impoverishment  of  the 
blood  reaches  this  minimum  hmit,  it  can  go  no  further  mthout 
damage  to  the  organism;  and  consequently  if  the  lessened 
intake  of  food  continues  the  total  volume  of  the  blood  must 
be  lessened,  in  order  that  the  minimum  limit  be  not  passed. 

It  is  possible  that  this  law  of  an  irreducible  minimum 
may  hold  for  many  of  the  constituents  of  the  blood,  and  that 
the  high  diaphragm  of  neurasthenia  is  due  to  the  deficiency 
in  the  blood  of  some  chemical  substance,  or  some  internal 
secretion.  The  case  I  have  already  referred  to  of  the  labourer 
who  suffered  from  neurasthenic  sj^mptoms,  and  had  a  high 
diaphragm,  and  was  cured  by  the  administration  of  thyroid 
gland,  seems  to  point  towards  such  a  possibility. 

High  Diaphragm  from  Heart  Weakness 

Further  evidence  can,  however,  be  adduced  in  favour  of 
this  proposition  that  a  lessening  of  the  amount  of  blood  in 
circulation  through  the  lungs  and  heart  causes  a  recognisable 
diminution  in  their  total  bulk,  and  is  followed  by  a  rise  in  the 
diaphragm. 

The  volume  of  the  blood  cu'culating  through  the  lungs 


DIMINISHED  BLOOD  VOLUME  181 

is  not  dependent  solely  upon  the  total  volume  of  the  blood  in 
the  body  ;  it  is  also  dependent  upon  the  strength  of  the  heart. 

A  decided  weakening  of  the  heart  as  a  whole  might  reason- 
ably be  expected  to  diminish  the  volume  of  blood  circulating 
through  the  lungs.  If  a  diminution  of  the  total  volume  of 
the  blood  in  circulation  causes  such  emptiness  of  the  lungs 
and  vessels  that  the  diaphragm  has  to  rise  so  as  to  adjust 
the  size  of  the  thorax  to  the  diminished  bulk  of  its  contents, 
theii  this  same  phenomenon  would  also  occur  if  a  weakening 
of  the  heart  muscle  results  in  an  automatic  diminution  in  the 
amount  of  blood  in  circulation  in  order  to  accommodate,  as 
far  as  possible,  the  bm-den  to  the  heart's  power  of  bearing  that 
burden.  There  is  good  clinical  evidence  that  this  takes  place, 
for  marked  cardiac  asthenia  is  extremely  frequently  accom- 
panied by  a  rise  in  the  level  of  the  diaphragm. 

This  phenomenon  of  high  diaphragm  would  not,  however,  be 
expected  in  cases  in  which  cardiac  weakness  is  accompanied  by 
fullness  of  the  veins — such  as  cases  of  failing  compensation.  In 
cases  of  valvular  disease,  nevertheless,  the  level  of  the  diaphragm 
ought  to  be  watched,  as  it  may  give  very  important  indications. 

Such  a  sudden  weakening  of  the  heart  with  a  fall  in  the 
strength  of  the  pulse  is  a  well-known  sign  of  the  onset  of  peri- 
carditis, and  when  this  takes  place  in  a  young  patient  whose 
fibrous  tissues  have  not  yet  become  unyielding  a  well-marked 
rise  in  the  level  of  the  diaphragm  will  be  found  to  be  present. 

This  rise  is  especially  noticeable  where  failure  of  the  heart 
muscle  from  myocarditis  or  pericarditis  occurs  as  a  complica- 
tion of  rheumatic  fever ;  for  the  rheumatic  poison  causes  a 
softening  of  fibrous  tissues,  allowing  the  displacement  of  organs 
to  occur  more  readily  than  if  rheumatism  were  not  present. 

I  give  an  illustration  of  an  extreme  case  of  this  type. 

The  gastric  resonance  reached  as  high  as  the  lower  border  of 
the  fourth  rib  on  the  left,  and  the  relative  liver  dullness  reached 
the  upper  border  of  the  third  rib  in  the  right  nipple  Une,  the 
lower  edge  of  the  liver  dullness  being  at  the  lower  edge  of  the 
sixth  rib  (Case  XI,  figs.  39  and  40).  When  the  heart  recovered, 
some  eighteen  days  later,  the  gastric  resonance  and  the  liver 
dullness  had  both  returned  to  the  normal  level.  The  details 
of  the  case  are  as  follows  : — 


182 


HIGH  DIAPHRAGM  A  SIGN  OF 


Case  XL — Rheumatic  Pericarditis 

Emily  E.,  aged  fifteen,  was  admitted  on  October  29,  very- 
ill  with  rheumatism  and  pericarditis. 

The  diaphragm  was  very  high,  the  gastric  resonance  reach- 
ing to  the  fom-th  rib,  and  the  relative  dullness  of  the  liver  was 
at  the  third  rib  in  the  right  nipple  line.  The  lower  edge  of 
the  hver  only  reached  to  the  lower  border  of  the  sixth  rib. 
Three  weeks  later,  on  November  20,  the  condition  had  improved, 

■ .  VL '.    ■"  -  !*■ '         High  Diapheagm  in  Pericarditis 


Relative  dulness. 
with  full    '  '  ^ 
expirdtion 


Fig.  39. — Case  XI :  Pericarditis. 

November  20.     Very  high  right  diaphragm. 


Fig.  40.— Case  XL 

December  8.    Konnal  again. 


but  the  diaphragm  was  still  high,  as  shown  in  fig.  39.  Within 
another  three  weeks  the  diaphragm  was  nearly  back  to  its 
normal  level  (see  fig.  40). 

There  was  very  considerable  dilatation  of  the  right  ventricle 
upwards  to  the  left  in  this  case. 

A  similar  well-marked  case  was  one  in  which  sudden  myo- 
cardial weakness  occm-red  in  a  case  of  influenza  complicated 
by  acute  colitis. 

Case  X. — Influenza 

The  heart  weakness  showed  itself  by  a  sudden  fainting 
attack,  during  which  the  heart-rate  fell  to  40,  and  even  to  as 
low  as  30  for  a  short  time,  if  the  pulse-rate  were  to  be  trusted. 
The  cardiac  asthenia  was  so  extreme  that  for  a  fortnight  or 


DIMINISHED  BLOOD  VOLUME 


183 


High  Diaphragm  in  Myocardial 
Weakness 


more  the  patient  dare  not  raise  his  arms  for  fear  of  bringing  on 
a  fainting  attack.  During  this  time  the  diaphragm  rose  steadily. 
In  spite  of  the  fact  that  the  patient  was  a  young  man,  with 
voluminous  lungs  (due  to  his  playing  a  wind  instrument  as  a 
pastime),  the  gastric  resonance  on  the  fourth  day  of  the  ill- 
ness reached  into  the  fifth  left  intercostal  space,  and  by 
the  twelfth  day  reached  the  middle  of  the  fifth  rib  in  the  left 
nipple  hne.  Similarly,  the  absolute  liver  dullness  by  the  twelfth 
day  had  risen  from  the  sixth  interspace  to  the  lower  border  of 
the  fifth  rib.  Accompanying  this  rise  in  the  diaphragm  there 
was  a  marked  diminution 
in  the  cardiac  dullness  :  in 
fact,  it  almost  entirely  dis- 
appeared, there  being  on 
the  twelfth  day  of  the  illness 
no  absolute  dullness,  and 
only  a  little  relative  dull- 
ness in  the  fourth  space, 
internal  to  the  nipple  line 
but  not  reaching  to  the 
sternum. 

Here,  then,  we  had 
marked  cardiac  asthenia 
associated  with  a  rise  in  the 
diaphragm  and  diminution 
in  the  size  of  the  cardiac 
dullness. 

Within  five  weeks  of  this 
date  the  gastric  resonance 
was  back  at  the  normal 
level,    and    there    were    4 

inches  of  cardiac  dullness  in  the  fourth  interspace  instead  of 
under  2  inches,  as  on  the  date  above  mentioned,  and  the 
heart  was  much  stronger.  The  patient  made  a  perfect 
recovery,  although  appendicitis  supervened  on  the  acute 
colitis. 

Clinical  Significance  of  High  Diaphragm 

As  regards  the  chnical  significance  of  high  diaphragm, 
the  question  has  of  necessity  been  dealt  with  in  the  above 
discussion  of  the  phenomenon.  It  is  an  important  danger 
signal  in  some  cases  of  severe  enteric  fever.     It  is  a  useful 


ormal 


Fig.  41.— Case  X. 
High  diapliragm  in  sudden  cardiac  failure. 


134  HIGH  DIAPHRAGM 

guide  as  to  the  extent  to  which  rectal  feeding  may  be  pushed. 
It  must  also  be  borne  in  mind  because  in  cases  of  suspected 
rupture  of  a  gastric  ulcer  the  absence  of  the  liver  dullness 
cannot,  as  is  now  well  recognised,  be  relied  on  as  an  indication 
of  free  gas  in  the  peritoneal  cavity. 

In  heart  disease  also  the  level  of  the  diaphragm  is  a  useful 
guide  as  to  the  condition  of  the  circulation.  If  the  weakness 
of  the  heart  muscle  be  the  prime  factor,  we  shall  expect  a  high 
diaphragm,  unless,  as  in  advanced  age,  the  tissues  be  too  rigid 
to  yield  easily  ;  if,  on  the  other  hand,  some  obstruction  to  the 
circulation — such  as  valvular  defect — be  the  chief  cause  of 
failure,  there  will  be  excess  of  blood  in  the  veins  of  the  thorax, 
and  a  normal  or  a  low  diaphragm  would  be  found. 

Thus  we  have  in  the  height  of  the  diaphragm,  as  shown 
by  the  upper  level  of  the  gastric  resonance,  an  indication  for 
treatment  and  a  help  in  the  diagnosis  and  prognosis  of  disease, 
with  which  we  can  ill  afford  to  dispense. 


Essay  III.— DIMINUTION  IN  THE  AEEA  OF  THE 
LIVEE  DULLNESS  AS  AN  IMPOKTANT  SIGN  OF 
MYOCAEDIAL  WEAKNESS  OE  OF  DEFICIENCY 
IN  THE  TOTAL  VOLUME  OF  THE  BLOOD  ^ 

Diminution  of  the  Liver  Dullness  due  to  Heart 
Weakness 

The  subject  of  muscular  failure  of  the  heart  is  too  apt  to 
to  be  dealt  with  in  our  text-books  of  the  present  day  in  its 
more  extreme  and  easily  recognisable  degrees,  rather  than 
in  its  earlier  ones.  Too  little  is  said,  and  perhaps  known, 
as  to  those  signs  which  show  that  the  tide  has  just  turned  in 
the  wrong  direction.  The  important  thing  in  dealing  with 
cardiac  failure  is  to  look  for  the  straws  which  show  the  first 
change  in  the  direction  of  the  current,  and  not  to  wait  until  the 
current  is  evidently  running  strongly  in  the  wrong  direction. 

If  cardiac  failure  is  not  recognised  till  marked  breathless- 
ness,  enlargement  of  the  liver,  and  dropsy  have  commenced, 
most  valuable  time  has  been  lost. 

Among  the  recognised  methods  of  ascertaining  the  working 
power  of  the  heart  there  are  very  few  which  give  us  information 
as  to  the  early  commencement  of  pure  muscular  failure.  In 
such  cases  reliance  is  mainly  placed  upon  the  patient's  sub- 
jective symptoms ;  but  yet,  valuable  though  these  be,  some 
surer  guide  in  the  way  of  objective  signs  of  muscular  failure 
are  highly  desirable.  Our  recognised  armamentarium  is  un- 
fortunately very  poor  in  such  signs,  in  spite  of  the  fact  that 
they  are  by  no  means  non-existent. 

They  are  mainly  to  be  looked  for  among  phenomena  due 
to  deficient  fullness  of  both  the  arterial  and  the  venous  system, 

^  Subject  of  a  communication  to  the  Dublin  Meeting  of  the  Association  of 
Physicians,  June  1909. 

185 


186  SMALL  LIVER  DULLNESS 

in  contradistinction  to  mechanical  failure  of  the  heart  where 
emptiness  of  the  arterial  system  is  associated  with  fullness  of 
the  veins. 

The  clinical  study  of  myocardial  failure  seems  to  prove 
that  when  the  heart  muscle  is  weak,  the  volume  of  blood  in 
circulation  is  cut  down  so  as  to  apportion  the  work  to  be  done 
to  the  heart's  power  of  doing  it. 

What  happens  to  this  blood,  which  is  cut  out  of  the  cir- 
culation by  the  regulating  mechanism  of  the  body,  I  am  not 
as  yet  prepared  to  say,  as  I  have  not  yet  been  able  to  take 
up  the  investigation.  In  acute  heart  failure  there  can  be  no 
doubt  that  the  blood  is  simply  stored  aw^ay  in  the  abdominal 
veins  or  other  reservoir's.  In  cases  where  the  onset  of  heart 
weakness  is  more  gradual  and  permanent,  it  is  probable  that  the 
actual  volume  of  blood  in  the  body  is  diminished. 

Also  in  these  cases  there  is  some  interesting  work  to  be 
done  in  answer  to  the  question  :  Does  the  specific  gravity 
of  the  blood  and  its  corpuscular  richness  rise,  owing  to  the 
eHmination  of  water  only  from  the  blood,  in  a  case  of  acute 
heart  weakness  where  the  condition  persists,  or  is  there  a 
continuous  storage  without  any  concentration  of  the  blood 
in  active  circulation,  until  the  volume  of  the  blood  can  be 
lessened  by  diminished  activity  of  the  blood-forming  glands  ? 

In  slowly  developing  myocardial  weakness  the  diminution 
will  probably  be  brought  about  by  diminished  formation  of 
blood. 

Whatever  the  answer  to  these  theoretical  questions,  the 
clinical  fact  remains  that  in  heart  weakness  of  pure  muscular 
origin,  apart  from  overstrain — absolute  or  relative — there 
is  abundant  evidence  of  diminution  in  the  volume  of  the 
cii'culating  blood. 

The  most  valuable  signs  are  those  associated  with  emptiness 
of  the  vascular  system,  especially  upon  the  venous  side. 

Of  these  the  most  important  are  a  series  of  signs  due  to  a 
diminution  in  the  volume  of  the  heart,  lungs,  and  Hver,  when 
the  blood  passing  through  them  is  lessened  in  volume,  smallness 
of  the  heart  and  liver  being  recognisable  by  percussion,  and 
diminution  in  the  size  of  the  lungs  and  intrathoracic  blood- 
vessels being  measured  by  the  altered  position  of  the  dia- 


IN  HEART  WEAKNESS  187 

phragm,  and  by  hollowing  above  the  clavicles  in  cases  where  the 
diaphragm  is  not  very  elastic. 

The  hoUowness  above  the  clavicle  and  smallness  of  the 
veins  in  myocardial  failure  form  a  striking  contrast  to  the 
fullness  and  pulsation  seen  in  valvular  disease,  and  other  cases 
of  mechanical  failure,  apart  from  weak  heart  muscle. 

In  addition  to  these,  there  are  certain  signs  of  emptiness 
of  the  arterial  system — such  as  pallor,  which  is  only  present 
in  special  cases — and  breathlessness,  from  weakness  of  the  right 
ventricle.  Also,  not  infrequently,  cases  are  met  with  where 
the  left  ventricle  is  relatively  weaker  than  the  right,  and  in 
such  a  case  it  is  not  breathlessness  which  prevents  the  patient 
walking  far  or  going  up  hills,  but  leg  weariness — an  aching  pain 
in  the  calves,  which  gets  worse  the  longer  he  walks,  and  which 
forces  him  to  stop  and  rest — an  '  intermittent  claudication, ' 
so-called,  of  pm-e  myocardial  origin. 

By  far  the  most  valuable  of  these  signs  are  those  afforded 
by  diminution  in  the  size  of  the  heart,  the  lungs,  and  the  liver. 

The  diminished  volume  of  the  intrathoracic  viscera,  as 
measured  by  a  rise  in  the  position  of  the  diaphragm  was  dealt 
with  at  pp.  163  etseq.,  and  it  only  remains  for  me  to  say  here 
that  enough  stress  is  not  laid  in  our  text-books  upon  the  dimin- 
ution in  the  size  of  the  heart,  which  may  be  detected  by 
careful  percussion.  Enlargement  of  the  heart  is  recognised  as 
an  important  sign  of  altered  heart's  action,  but  diminution  in 
its  size  is  less  apt  to  be  recognised  as  a  sign  of  muscular  weakness 
than  its  importance  deserves  {vide  figs.  42-52,  and  fig.  53). 

In  this  paper,  I  shall  deal  with  indications  given  by  diminu- 
tion in  the  size,  real  or  apparent,  of  the  liver  as  judged  by 
careful  percussion  of  its  areas  of  dullness,  absolute  and  relative. 

It  is  only  within  the  last  two  years  or  so  that  the  fact  of 
this  diminution  and  its  clinical  importance  were  brought  home 
to  me,  and  my  enlightenment  came  through  the  careful  mapping 
out  of  the  hepatic  dullness,  for  the  purpose  of  illustrating 
alterations  in  the  level  of  the  diaphragm.  The  diagrams 
were  accurately  drawn  from  nature,  and  doubtless  many  of 
those  reading  the  paper  on  that  subject  (which  is  reprinted 
verbatim  in  the  previous  essay)  felt,  as  I  did,  that  the 
explanations    given   are    not    adequate  to   fully   explain  the 


188  SMALL  LIVER  DULLNESS 

appearances  presented  by  many  of  them.  They  abundantly 
proved  my  thesis  as  to  the  rise  of  the  diaphragm  in  cardiac 
weakness  ;  but  the  variations  in  the  size  of  the  liver  dullness 
were  greater  than  could  be  accounted  for  by  the  variations 
in  the  position  of  the  diaphragm.  It  was  on  trying  to  under- 
stand my  own  diagi-ams  that  a  truth  came  upon  me  which,  to 
the  best  of  my  knowledge,  has  not  as  yet  been  recognised 
by  the  medical  profession,  but  which  ought,  ever  since  the 
days  when  percussion  was  first  used,  to  have  been  peifectly 
patent  to  every  one.  So  blind  are  we,  and  so  little  able  to 
leave  the  ruts  along  which  we  roll  too  contentedly  all  our 
lives  ! 

We  know  that  the  liver  is  an  elastic  organ,  and  that,  when 
there  is  over-distension  of  the  right  auiicle  and  the  gi'eat 
veins,  it  may  rapidly  enlarge,  till  it  is  double  its  noimal  size, 
and  then  subside  again  when  the  heart  recovers  itself,  and 
the  engorgement  of  the  right  heart,  &c.,  is  lessened. 

We  know  that  the  liver  is  elastic,  and  distends  when  over- 
filled with  blood,  but  we  never  thought  of  examining  to  see 
whether  the  elasticity  of  the  liver  did  not  lead  it  to  relax  and 
diminish  in  volume  when  it  was  under-filled  wdth  blood,  owing 
to  the  weakness  of  the  heart's  action,  or  other  cause. 

I  am  surprised  to  think  that,  durmg  the  first  twenty-four 
years  that  I  carefully  studied  the  abnormalities  due  to  disease 
in  the  human  mechanism,  I  never  (until  the  year  KO'/)  made 
this  simple  deduction.  I,  in  common  with  my  brother 
practitioners,  constantly  noticed  marked  diminution  in  the 
amount  of  liver  dullness  ;  often  found  the  intestinal  resonance 
well  above  the  level  of  the  costal  arch  on  the  right  side,  and 
yet  passed  the  observation  by,  because  I  did  not  know  the 
meaning  of  it,  and  did  not  take  the  mental  trouble  of  saying  : 
'  Why  is  the  area  of  liver  dullness  lessened  ?  ' 

I  now  know  that  diminution  in  the  area  of  the  Hver  dullness 
is  a  most  valuable  sign  of  heart  weakness. 

The  principle  underlying  this  diminution  in  the  size  of  the 
organs,  we  have  referred  to,  may  be  stated  as  a  general 
proposition. 

Marked  variation  in  the  actual  volume  of  the  heart  and  of 
the  more  vascular  of  the  elastic  solid  viscera,  both  as  regards 


IN  HEART  WEAKNESS  189 

increase  or  decrease,  occuis  as  a  result  of  variation  in  the 
amount  of  work  which  the  heart  is  doing,  or  in  the  amount  of 
blood  which  is  being  kept  in  circulation  by  it. 

Where  the  actual  size  of  these  organs  can  be  determined 
by  clinical  methods,  valuable  information  as  to  the  state  of 
the  heart  and  circulation  can  thereby  be  gained. 

There  is,  I  think,  little  doubt  that  there  will  be  some  varia- 
tion in  the  size  of  the  spleen,  and  possibly  also  of  the  kidneys  ; 
but  as  theii"  size  is  not  easily  definable  by  our  present  clinical 
methods,  any  variation  in  their  size  is  of  no  value  to  the  clinician. 

Percussion  of  the  Liver 

For  the  detection  of  changes  due  to  variation  in  the  size 
of  the  hver  it  is  best  to  map  out,  by  means  of  percussion,  the 
area  of  absolute  hver  dullness,  with  the  patient  recumbent 
on  his  back.  It  is  also  interesting  to  follow  the  outhne  of 
the  relative  dulhiess  by  means  of  firm  percussion,  where  it 
underhes  the  edge  of  the  lung,  and  light  percussion  where  it 
overhes  the  resonant  intestine. 

When  mapped  out  in  this  position,  it  is  not  mfrequent 
to  find  that  there  is  no  absolute  dullness  at  all,  internal  to  the 
right  nipple  line — the  normal  dullness  of  the  left  lobe  of  the 
liver  disappearing,  as  well  as  most  of  the  anterior  part  of 
the  right  lobe.  In  such  a  case,  instead  of  the  hver  dullness 
reaching  to  the  costal  arch  in  the  nipple  hne,  and  crossing 
a3ross  the  middle  hne  below  the  xiphoid  cartilage,  there  will 
be  full  intestinal  or  gastric  resonance  for  some  1|  or  2  inches 
above  the  costal  arch,  and  the  gastric  resonance  will  meet  the 
lung  resonance  in  the  middle  line  {vide  figs.  51  and  55). 

There  are  probably  four  factors  which  may  aid,  in  varying 
degree,  in  producing  this  disappearance  of  the  liver  dullness 
anteriorly. 

(1.)  In  the  first  place,  there  is  shrinkage  in  the  absolute 
volume  of  the  Hver,  due  to  abnormal  emptiness  of  its  veins 
and  arteries.  Judging  by  the  mechanism  whereby  the  Hver 
enlarges  when  overfuU  of  blood,  the  hepatic  vein,  aided  by 
the  portal  vein,  will  play  a  more  important  part  than  the 
arterial  system. 


190  SMALL  LIVER  DULLNESS 

(2.)  A  second  factor  plays  quite  as  important  a  part  as  the 
one  just  mentioned,  and  probably  a  more  important  one — 
namely,  the  loss  of  firmness  which  results  from  its  insufficient 
distension  with  blood. 

When  once  the  elastic  nature  of  the  liver  is  grasped,  this 
flaccidity  of  the  under-filled  organ  is  easily  understood. 

When  the  patient  is  lying  on  his  back,  this  flaccidity 
probably  causes  the  anterior  edge  of  the  Hver  to  fall  away 
from  the  chest  wall,  and  so  enable  the  air-containing  intestines 
to  come  in  contact  with  the  ribs  above  the  costal  arch.  In  this 
connection  it  must,  however,  be  remembered  that  when  the 
edge  of  the  liver  is  thin,  it  is  not  easy  by  percussion  to 
distinguish  it  from  underlying  air-filled  intestines. 

It  is  sometimes  quite  easy  to  demonstrate  this  flaccidity. 
Thus,  take  a  patient  of  this  type,  where  there  is  no  absolute 
dullness  internal  to  the  right  nipple  line,  when  on  his  back, 
and  then  make  him  sit  up  and  lean  weU  forward.  It  wiU  then 
be  found  that  the  liver  dullness  occupies  its  normal  situation 
anteriorly,  but  that  there  is  intestinal  resonance  posteriorly, 
where  liver  dullness  ought  to  be  {vide  Case  VI,  fig.  55). 

(3.)  The  third  factor  is  that  to  which  I  referred  in  the  essay 
on  the  Rise  of  the  Diaphragm — namely,  the  altered  relation- 
ships of  the  liver  anteriorly,  which  result  from  a  rise  in  the 
level  of  the  diaphragm. 

With  a  normal  Uver  and  a  normal  diaphragm,  the  anterior 
edge  of  the  liver  will  reach  the  costal  arch  in  the  right  nipple 
line,  and  as  far  down  as  the  seventh  rib.  When,  however,  the 
arch  of  the  diaphragm  rises,  owing  to  a  shrinkage  of  the  thoracic 
viscera,  the  posterior  fixation  of  the  liver  prevents  its  rising 
up  into  the  arch  of  the  diaphragm  as  a  whole,  and  therefore 
the  loose  anterior  margin  and  the  left  lobe  have  to  rise  out  of 
proportion  to  the  rest  of  the  liver,  and  consequently  do  not 
reach  as  low  down  anteriorly  as  formerly,  being  drawn  back, 
as  it  were,  under  the  diaphragm.  In  the  case  of  a  very  high 
diaphragm,  it  is  conceivable  that  the  left  lobe  of  the  liver, 
and  the  anterior  margin  of  the  right  lobe,  may  not  be  able 
to  reach  the  anterior  chest  waU  at  all,  being  entirely  under 
the  arch  of  the  diaphragm. 

This  third  factor  does  play  a  very  important  part,  combined 


IN  HEART  WEAKNESS  191 

with  the  others  (especially  the  first),  in  the  production  of  the 
more  extreme  cases  of  disappearance  of  the  liver  dullness 
anteriorly.  Nevertheless,  a  very  considerable  loss  of  liver 
dullness  without  much  evidence  of  a  rise  in  the  diaphragm 
is  by  no  means  infrequent. 

(4.)  The  fom-th  factor  ^  is  the  altered  conductivity  to  percus- 
sion vibrations,  which  appears  to  accompany  relaxation  of 
the  liver  tissue.  It  is  extremely  probable  that  the  main  reason 
for  the  disappearance  of  the  liver  dullness  when  the  organ 
is  underfilled  with  blood  is  that  when  it  is  sufficiently  flaccid 
the  Hver  tissue  loses  its  power  of  damping  down  the  resonance 
of  the  underlying  stomach  and  intestines.  Over- distension  of 
the  hver  tissue  with  blood  certainly  has  this  effect,  and  if  it 
could  be  proved  that  under-filling  and  flaccidity  also  increased 
the  conductivity  of  the  liver  tissue  to  the  percussion  vibra- 
tions of  subjacent  resonant  viscera,  it  would  explain  the 
regular  and  sometimes  extreme  variations  in  the  area  of 
absolute  liver  dullness  far  better  than  either  of  the  foregoing 
theories.  It  is  sometimes  possible  to  note  a  complete 
disappearance  of  the  absolute  liver  dullness  as  far  back  as 
the  anterior  axillary  line.  In  such  a  case  the  intestinal 
resonance,  on  firm  percussion,  comes  right  up  to  the  lung 
resonance  as  far  out  as  the  anterior  axUlary  line.  It  is  incon- 
ceivable that  there  can  be  a  sufficient  diminution  in  the  actual 
size  of  the  liver  to  account  for  this  phenomenon,  and  it  is  not 
easy  to  conceive  how  it  could  be  due  to  a  falling  away  of  the 
liver  tissue  from  the  chest  wall  owing  to  flaccidity.  Moreover, 
the  relationship  of  the  relative  to  the  absolute  dullness  along 
the  lower  edge  of  the  liver  does  not  altogether  suggest  the 
falling  back  of  the  edge  of  the  liver  and  the  substitution  close 
to  the  abdominal  wall  of  resonant  intestines  instead  of  dull 
liver  tissue.  The  way  the  resonance  shades  off  into  the  dullness 
suggests  altered  conductivity  as  the  cause  of  the  intestinal 
resonance  taking  the  place  of  liver  dullness. 

This  same  explanation  is  also  suggested  by  the  complete 
disappearance  of  the  dullness  due  to  the  left  lobe  of  the  hver. 
This  IS  very  often  noticed  in  heart  weakness  or  malnutrition, 

^  This  fourth  factor  was  only  realised  as  a  possibility  by  the  writer  in 
December  1913. 


192  SMALL  LIVER  DULLNESS 

and  it  seems  more  likely  that  it  results  from  altered  conduc- 
tivity rather  than  that  the  left  lobe  so  diminishes  in  size 
as  to  be  able  to  fall  back  completely  under  the  arch  of  the 
diaphragm. 

Moreover,  if  the  disappearance  were  entirely  due  to  a 
falling  away  of  the  liver  when  the  patient  was  lying  back,  a 
reversal  of  his  position  would  not  only  restore  the  liver  dullness, 
but  also  give  an  abnormal  amount. 

On  making  this  observation  it  is  found  that  sometimes 
the  liver  dullness  returns  anteriorly  when  the  liver  is  percussed 
while  the  patient  is  on  his  hands  and  knees,  and  at  the  same 
time  disappears  posteriorly — as  would  be  the  case  if  flaccidity 
were  the  main  cause  of  the  disappearance  of  the  hver  dullness. 
In  this  attitude,  the  falling  forwards  of  the  flaccid  liver  would 
restore  the  dullness  anteriorly  and  allow  the  resonant  intestines 
to  reach  the  ribs  posteriorly. 

On  the  other  hand,  tliis  experiment  does  not  always  give 
this  result  and  often  the  increase  in  the  dullness  anteriorly  is 
by  no  means  as  great  as  would  be  the  case  if  the  disappearance 
had  been  due  to  flaccidity  of  the  liver  tissue  alone. 

If  this  theory  of  altered  conductivity  proved  to  be  correct, 
the  following  generalisation  can  be  made. 

The  power  which  the  liver  tissue  possesses  of  damping 
down  the  resonance,  which  underlying  air -containing  viscera 
would  give  on  percussion,  and  thus  giving  rise  to  the  dull  note 
which  is  called  the  absolute  liver  dullness,  depends  upon  the 
tension  of  its  tissue  as  well  as  upon  the  thickness  of  tissue 
which  overlies  the  resonant  organ. 

This  power  of  damping  down  percussion  vibrations  and 
giving  a  dull  percussion  note  is  lessened  whenever  the  tension  of 
the  Hver  tissue  is  either  increased  or  diminished  beyond  a 
certain  point.  In  other  words,  when  the  hver  tissue  is  more 
tense  or  more  flaccid  than  normal  its  power  of  conducting 
percussion  vibrations  is  increased,  and  it  seems  as  if  the  increase 
of  conductivity  were  proportional  to  the  extent  of  the  departure 
from  the  normal  tension  of  the  hver  tissue  as  regards  both 
excess  and  defect. 

If  this  be  so,  it  can  be  asserted  that  the  liver  loses  to  some 
extent  its  power  of  damping  down  the  resonance  of  the  under- 


IN  HEART  WEAKNESS  193 

lying  viscera  when  its  normal  tension  is  either  sufficiently 
increased  by  over-distension  of  its  vessels  with  blood  or  lowered 
by  their  under-filling. 

The  extent  of  the  over-filhng  and  congestion  can  be 
estimated  by  the  extent  to  which  the  area  where  the  liver 
gives  an  absolutely  dull  note  retreats  back  from  the  edge  of 
the  hver  as  determinable  by  palpation. 

Also  the  extent  of  the  under -filling  of  the  hver  with  blood 
can  be  estimated  by  the  extent  to  which  the  area  of  absolute 
dullness  diminishes,  and  its  retm-n  towards  normal  conchtions 
by  the  retm*n  of  the  absolute  liver  dullness  towards  its  normal 
size. 

The  careful  study  of  a  long  series  of  cases — such  as  I  have 
not  yet  had  time  to  make — will  probably  make  it  possible  to 
differentiate  between  the  part  played  by  each  of  these  three 
factors  in  any  particular  case. 

Changes  due  to  flaccidity  are,  as  already  pointed  out, 
distinguishable  by  the  effect  of  change  of  position.  Further, 
so  far  as  my  present  observations  go,  I  can  make  the  sugges- 
tion that  the  presence  of  some  dullness,  absolute  or  even 
relative,  in  the  situation  of  the  left  lobe  of  the  liver,  together 
with  a  narrow  strip  of  dullness  joining  it  with  the  rest  of  the 
hver  dullness  on  the  right  side,  would  suggest  rather  the 
presence  of  relaxation  of  the  hver  tissue  than  actual  shrinkage 
— with  or  without  high  diaphi-agm.  In  cases  where  the 
liver  dullness  is  absent  in  and  to  the  left  of  the  middle  hne, 
there  is  almost  certairdy  shrmkage  with  or  without  high 
diaphragm. 

We  may  learn  something  as  to  the  condition  of  the  Hver, 
so  far  as  the  presence  or  absence  of  fibrous  tissue  is  concerned, 
when  we  come  to  know  more  as  to  the  meaning  of  the  very 
various  shapes  which  we  find  that  the  hver  dullness  assumes 
when  diminishing  in  volume  owing  to  circulatory  changes. 

I  need  hardly  say  that  I  exclude  from  the  scope  of  these 
remarks  any  cases  where  there  is  a  probability  that  the  lessened 
size  of  the  hver  is  of  organic  origin,  and  due  to  cirrhosis  or 
other  definite  lesion.  In  the  cases  upon  which  this  paper 
is  based  the  shrinkage  was  of  transient  nature,  lasting  only 
a  few  days  or  weeks. 


194  SMALL  LIVER  DULLNESS 

Diminution  in  the  Area  of  the  Liver  Dullness  due  to 
Deficiency  in  the  Total  Volume  of  the  Blood 

When  dealing  with  changes  due  to  deficient  distension  of 
the  organs  with  blood,  it  must  be  remembered  that  a  cir- 
culatory failure  of  this  nature  may  not  only  result  from 
weakness  of  the  pump  :  it  will  also  result  from  a  deficiency 
in  the  liquid  pumped. 

We  therefore  see  precisely  the  same  changes  in  the  Hver, 
as  those  just  described,  in  cases  where  the  heart  is  not  at  fault, 
but  where,  as  in  the  case  of  severe  haemorrhage,  there  is  a 
lessening  in  the  total  volume  of  the  blood,  and,  consequently, 
the  capacity  of  the  whole  vascular  system  must  be  lessened 
in  order  that  the  proper  blood  pressure  may  be  maintained 
within  it.  Such  a  lessenuig  of  the  total  volume  may  also  take 
place,  as  clinical  observation  proves,  owing  to  a  deficiency 
in  the  body  of  some  of  the  essential  constituents  of  the  blood, 
for  in  the  presence  of  such  a  deficiency  the  total  volume 
must  be  compensatorily  diminished,  in  order  that  the  proper 
percentage  composition  may  be  maintained.  The  simplest 
illustration  of  this  is  the  diminution  in  the  volume  of  the 
blood  which  takes  place  in  starvation. 

The  causes  of  the  shrinkage  of  the  liver  and  other  organs 
may  be  thus  summarised  : — 

Deficient  fullness  of  the  vascular  system,  resulting  in 
shrinkage  of  the  more  vascular  of  the  elastic  solid  viscera, 
results  from — 

I.  Failure  in  the  muscular  power  of  the  heart. 
IL  Deficiency  in  the  total  volume  of  the  blood,  due  to — 

1.  Actual  loss  of  blood  from  haemorrhage. 

2.  Loss  of  water  from  the  body — as  in  cholera,  &c. 

3.  Failure  of  the  blood-forming  organs,  or  excessive 
blood  destruction,  &c.,  causing  anaemia. 

4.  Compensatory  diminution  of  the  total  volume  of  the 
blood  in  order  to  maintain  at  its  proper  percentage  some 
essential  constituent  of  which  there  is  an  insufficient  amount 
in  the  body,  for  instance— 

(a)  Deficiency  of  ordinary  proteids  and  nutritive  materials* 
as  in  any  form  of  starvation. 


IN  HEART  WEAKNESS  195 

(h)  Deficiency  of  some  internal  secretion,  such  as  that  of 

the  thyroid  gland, 
(c)  Deficiency  of  special  materials  necessary  for  the  nutri- 
tion of  the  nervous  system. 
{d)  Defective  volume  of  the  blood  seen  in  cases  of  neuras- 
thenia without  malnutrition. 
In  addition  to  these  causes  of  variation  in  the  extent  of 
the  liver  dullness,  it  must  not  be  forgotten  that  in  a  very  small 
percentage  of  apparently  healthy  persons  the  diaphragm  may 
be  above  the  normal  line,  or  the  area  of  the  liver  dullness 
may  be  abnormally  small.     I  have  not  as  yet,  however,  met 
with  more  than  four  or  five  such  instances. 

The   clinical  aspects   of   diminution  in  the  liver   dullness, 
due  to  myocardial  weakness,  will  first  be  dealt  with. 


Diminution  of  Liver  Dullness  due  to  Myocaedial 
Weakness 

If  the  area  of  hver  dullness  and  the  outline— especially 
the  lower  border — of  the  cardiac  dullness  be  watched  carefully 
in  cases  such  as  acute  rheumatism,  where  there  is  risk  of 
weakening  of  the  myocardium  by  toxaemia  or  inflammation, 
some  very  instructive  observations  may  be  made,  and  the 
value  of  this  physical  sign  to  which  I  am  drawing  attention 
will  become  apparent. 

The  following  is  such  a  case  where  a  careful  record  of 
the  area  of  the  liver  dullness  and  of  the  cardiac  dullness 
showed  most  interesting  changes  taking  place  from  day  to 
day. 

I  give  a  large  number  of  figures  shomng  the  changes  that 
took  place  in  this  case ;  for  they  are  aU  more  or  less  character- 
istic of  what  may  be  found  in  cases  of  cardiac  weakness  with 
and  without  dilatation  of  the  right  ventricle,  and  also  in  cases 
where  the  liver  dullness  is  diminished  from  circulatory  causes 
other  than  cardiac  weakness  (see  figs.  42-52). 

Case  I. — The  patient  was  a  young  man  aged  about  twenty. 
When  first  seen,  he  had  been  under  treatment  for  ten  days  for 

o2 


Case  Showing  Variations  in  the  Size  of  the  Livee  Dullness  due  to 
Heaet  Weakness 


Fig,  42.— Case  I. 

May  16.  Acute  rheumatism.  Tem- 
perature 102°  P. ;  pulse  110.  Liver 
small ;    diaphragm  high. 


Fig.  43. — Case  I. 

May  18.  Much  better  after  full 
doses  of  sodium  salicylate,  but  dia- 
phragm higher  and  heart  and  Uver 
smaller. 


Fia.  44.— Case  I. 

May    20.      Still   improving, 
larger ;  diaphragm  lower. 


Fig.  45.— Case  I. 

Heart  May  23.     Better.     Heart,  liver,  and 

diaphragm  nearly  normal. 


Fig.  46. 


May  2G.  Heart  stronger,  but  the  thin 
part  of  the  right  ventricle  is  giving  way. 
Diaphragm  rising  again. 


Case  I. 


Slay  29.  Conus  of  right  ventriclo 
dilated,  but  Uver  larger  and  diaphragm 
lower. 


'  Fig.  48.— Case  I. 

June  1.  Right  ventricle  more  dilated, 
but  hver  larger  and  diaphragm  lower. 
Patient  better. 


Fig.  49.— Case  I. 

June  7.    Heart  smaller,  bat  patient 
not  so  well :  has  rheumatic  pain  again. 


198 


SMALL  LIVEK  DULLNESS 


acute  rheumatism,  by  ten-grain  doses  of  sodium  saKcylate, 
To  this  he  had  not  properly  responded,  for  the  joint  pain  and 
swelHng  was  still  considerable,  and  the  temperature  at  times 
reached  102°  F.  The  pulse  was  100-110.  There  was  mitral 
regurgitation  of  considerable  extent,  for  the  murmur  was  con- 
ducted down  the  spine  to  the  sacrum ;  the  apex  was  external 
to  the  nipple  line,  but  otherwise  the  heart  was  not  dilated  or 
enlarged. 

The  diaphragm  was  high,  and  the  absolute  liver  dullness 


Tig.  50.— Case  I. 

July  22.  Heart  and  liver  dullness 
smaller  and  diaphragm  higher  again. 
Fresh  endocarditis. 


Fig.  51.— Case  I. 

July  27.  Heart  larger,  Uver  dulhiess 
smaller.  Pull  doses  of  sodium  sulpho- 
carbolate  and  quinine. 


did  not  reach  the  costal  arch.  This  was  on  May  16,  and 
the  size  of  the  cardiac  and  hepatic  dullness  are  shown 
approximately  in  fig.  42. 

The  subsequent  diagrams  were  made — usually  by  the 
bed-side — after  carefully  percussing  out  the  areas  of  absolute 
and  relative  dullness  and  outlining  them  on  the  chest.  For 
such  work  as  this,  the  '  zinc  dust  and  aluminium  or  silver 
spatula  '  method  is  preferable  to  aniline  or  other  pencil,  from 
both  the  patient's  and  the  physician's  point  of  view. 

If  the  skin  be  rubbed  with  zinc  and  starch  dust,  it  is  then 
possible  to  mark  it  with  any  silver,  aluminium,  or  german- 
silver  spatula  or  letter-opener — just  as  if  one  were  waiting 
on  paper  with  a  lead  pencil.     I  am  indebted  to  the  father  of 


IN  HEART  WEAKNESS 


199 


this  particular  patient  for  working  out  the  explanation  of  this 
phenomenon,  and  I  do  not  think  it  has  hitherto  been  published. 
I  was  not  aware  of  the  explanation  when  I  described  this 
method  of  wiiting  on  the  skin  some  years  ago.  It  is  apparently 
purely  a  mechanical  phenomenon  ;  the  particles  of  zinc  oxide 
detach  particles  of  the  metal,  giving  what  is  technically  known 
as  '  a  streak,'  just  as  one  can  write  on  stone  with  a  piece  of 
metal.  The  sldn  can  also,  it  appears,  be  rendered  capable 
of  receiving  a  black  mark  from  a  soft  metal  point  if  it  be 
rubbed  with  such  a  material 
as  asbestos. 

I  have  heard  of  this 
property  of  the  sldn  —  of 
taking  impressions  from  the 
softer  metals  —  being  mis- 
takenly associated  with  trophic 


Fig.  52.— Case  I. 
August  15.    Patient  much  better  again. 


changes  occurring  in  paralysis 
of  various  kinds,  because  the 
chnical  teacher  in  question 
did  not  discover  that  the 
dermographic  power  was  not 
a  function  of  the  skin,  but 
of  the  '  ward-dust '  which  was 
applied  to  the  skin  of  the 
paralysed  parts  by  the  nurses 
in  charge  of  the  case. 

But  to  return  to  the  patient.  The  diagrams,  as  will  be 
seen,  were  taken  at  first  every  two  or  three  days,  and  subse- 
quently at  longer  intervals. 

Fig.  43  shows  a  decided  lessening  of  the  size  of  the  cardiac 
and  liver  dullness,  with  a  rise  in  the  diaphragm  of  an  inch  or 
more,  as  judged  by  the  level  of  the  gastric  resonance.  This 
may  have  been  due  to  the  continued  action  of  the  rheumatic 
poison,  or  it  may  have  been  due  to  the  w^eakening  of  the  heart 
caused  by  full  doses  of  sodium  salicylate  :  for  full  doses  are  often 
badly  borne  when  small  doses  have  been  given  for  some  time 
previously.  In  this  case  the  ultimate  result  was  good,  and  the 
next  two  figm-es  show  the  increasing  size  of  the  heart  and  lungs- 
Then  in  fig.  46  there  is  a  marked  change,  which  is  at  first  diffi- 
cult to  explain.     The  heart  had  been  steadily  improving  in  the 


200  SMALL  LIVER  DULLNESS 

strength  and  precision  of  its  sounds,  and  they  were  now  sharp 
and  good  ;  the  patient  also  was  feeling  better.  Wliy,  then,  the 
rise  in  the  diaphragm  and  the  gi'eat  diminution  in  the  liver 
dullness  which  this  diagram  shows  ? 

Another  change  is  also  shown — namely,  upward  increase  of 
the  cardiac  dullness,  which  was  combined  with  the  appearance 
of  pulsation  in  the  second  and  third  left  interspaces.  This 
gives,  I  think,  the  explanation. 

With  the  elimination  of  the  rheumatic  toxin,  the  muscular 
power  of  the  heart  had  increased,  but  the  tissues  of  the  heart 
were  still  much  below  their  normal  strength.  As  a  result,  the 
weakest  part  of  the  right  ventricle — ^namely,  the  so-called '  conus 
arteriosus  ' — being  unable  to  stand  the  rise  in  the  blood  pressm-e, 
had  begun  to  dilate. 

Nature  had  in  consequence — by  lessening  the  volume  of  the 
blood  in  circulation — endeavoured  to  lessen  the  strain  on  this 
weak  portion.  Hence  the  rise  of  the  diaphragm  and  the 
lessened  hepatic  dullness. 

The  next  two  figures  (47  and  48)  show  continued  improve- 
ment, and  in  the  latter,  which  was  taken  on  June  1 ,  the  relation- 
ships are  very  near  the  normal.  A  week  later,  there  was  a 
Httle  return  of  rheumatism,  calling  for  an  increased  dose  of 
salicin  and  accompanied  by  a  diminution  in  the  area  of  liver 
dullness  (fig.  49). 

By  the  end  of  June,  the  patient  was  much  better  and 
beginning  to  walk  about  a  little. 

This  improvement  was,  however,  soon  followed  by  a  relapse. 
The  heart  became  more  rapid  again ;  the  temperature  rose 
shghtly.  An  aortic  diastolic  murmur,  wliich  previously  had 
been  faint  and  indistinct,  was  now  well  marked,  showing  a 
recurrence  of  the  endocarditis. 

This  relapse  commenced  on  July  13,  and  was  well  marked  on 
the  22nd,  when  fig.  50  was  taken.  Figs.  50  and  51  both  show 
again  a  marked  diminution  in  the  size  of  the  cardiac  dullness 
with  a  rise  of  diaphragm  and  diminution  of  the  liver  dullness. 

On  July  22.  the  date  when  fig.  50  was  made,  he  had  been 
on  sodium  sulpho-carbolate"(gr.  xx)  every  two  hours,  together 
with  quinine  (gr.  ij)  every  two  hours  alternately.  At  this  time, 
he  was  beginning  to  show  some  physiological  symptoms  of  the 
action  of  each  of  the  drugs,  and  the  frequency  of  the  dose  was 
therefore  cut  down  to  every  three  hours,  with  some  omissions 
during  the  night.     On  this  dose  he  remained  till  his  recovery. 

Fig.  51,  taken  after   being  on  the  sulpho-carbolate  and 


IN  HEAET  WEAKNESS  201 

quinine  for  ten  days,  shows  a  remarkable  diminution  in  the 
left  lobe  of  the  liver  without  any  great  change  in  the  right. 

Fig.  52  show^s  the  condition  of  heart  and  liver  on  August  15, 
at  which  date  he  was  rapidly  gaining  weight  and  all  fear  of  his 
endocarditis  developing  into  septic  endocarditis  was  at  an 
end,  and  he  was  on  the  way  to  a  most  satisfactory  recovery  and 
with  a  heart  but  very  slightly  damaged. 

The  following  is  another  instance  of  the  important  informa- 
tion given  by  diminution  in  the  size  of  the  liver,  but  from 
the  opposite  extreme  of  cardiac  failure  as  compared  with 
the  last  case. 

Case  II. — The  patient  was  a  lady  of  forty-eight  years, 
with  mitral  regm-gitation  and  a  weak  and  dilated  heart  following 
influenza,  with  general  anasarca  threatening,  and  a  liver  down 
2  inches  below  the  costal  arch  from  venous  engorgement. 

One  day  it  was  found  that  the  liver  was  1|  inches  smaller 
than  it  had  been  two  daj^s  previously.  Was  this  a  sign  of 
improved  circulation  ?  It  might  have  been ;  but  here  it  was 
not  so,  for  the  patient  was  rather  worse  if  anything,  though  not 
markedly  so.  It  was  a  sign  of  failing  heart  muscle  and  a  call  for 
stimulation — albeit,  very  careful  stimulation,  owing  to  the  faulty 
nutrition  of  the  heart  muscle.  In  a  couple  of  days  the  hver 
had  returned  to  its  former  size,  and  the  threatened  danger  of 
heart  failure  had  been  averted.  Had  the  variation  in  the  size 
of  the  liver  not  given  timely  warning,  valuable  time  might  have 
been  lost  before  the  treatment  was  changed,  for  the  importance 
of  the  slight  alteration  in  the  patient's  symptoms  might  quite 
easily  have  been  overlooked  (see  also  p.  63). 

Instances  could  easily  be  multiplied  of  the  value  of  diminu- 
tion in  the  size  of  the  liver  dullness  as  indicating  cardiac  failm-e, 
and  it' is  specially  so  in  cases  of  myocardial  weakness  and 
degeneration.     The  following  is  an  instance: — 

Case  III. — The  patient,  a  man  aged  fifty-six,  had  suffered  for 
many  months  from  heart  weakness  and  persistent  high  tension, 
the  sphygmomanometer  showing  a  blood  pressure  of  210  mm. 
of  mercury,  as  a  rule.  One  day,  he  over-exerted  himself  physi- 
cally and  mentally,  and,  shortly  after  reaching  home,  became 
unconscious  and  had  a  slight  amount  of  right  hemiplegia.  The 
pulse  was  weak  and  rapid,  and  the  breathing  irregular  and 
almost  '  Cheyne  Stokes  '  in  character. 


202 


SMALL  LIVER  DULLNESS 


Was  the  case  one  of  cardiac  failure  or  of  cerebral 
thrombosis  ? 

On  examining  the  heart  there  was  almost  no  cardiac  dullness 
of  any  kind  to  be  detected,  and  an  extremely  feeble  impulse. 
There  was  no  fullness  of  the  neck  veins  and  no  absolute  liver 
dullness  in  the  middle  hne,  and  very  little  internal  to  the  right 
nipple  line.  Also  the  intestinal  resonance  could  be  obtained 
for  some  2  inches  above  the  costal  arch  where  the  liver  dullness 

ought  to  have  been. 

The  accompanying  dia- 
gram (fig.  53)  represents  with 
fair  accuracy  what  was 
found,  although  the  patient 
was  too  ill  to  admit  of 
accurate  notes  being  taken 
at  the  time.  It  will  be 
noticed  that  the  gastric 
resonance  reached  to  the 
fifth  rib,  showing  a  rise  of 
the  diaphragm  on  the  left 
side.  On  the  right  it  was 
within  the  normal  hmits. 

This  examination  of  the 
liver  showed  clearly  that 
the  cardiac  condition  was 
primary,  and  the  circulatory 
failure  in  the  brain  secondary. 
He  was  treated  as  a  case  of  myocardial  failure,  and  the 
brain  condition  rapidly  improved.  In  a  week  or  so  the  heart 
gained  strength  and  the  Hver  dullness  increased  in  volume 
reaching  to  the  costal  arch  and  being  also  absolute  in  the  middle 
hne.     The  cardiac  dullness  also  increased  in  size. 


Case  III. 


Small  heart  and  liver  dullness.     Heart  failure 
in  arterio-sderosis. 


II 


Clinical  Aspects  of  Diminution  of  the  Liver  Dullness 
DUE  TO  A  Shrinkage  in  the  Total  Volume  of  the 
Blood  in  Active  Circulation 

The  clinical  aspect  of  cases  where   the  scantiness  of  the 
circulating  blood  does  not  depend  upon  the  heart,  but  upon 


IN  SMALL  BLOOD  VOLUME  203 

an  actual  deficiency  in  the  l)loocl  itself,  must  now  be  briefly 
discussed. 

1.  Small  liver  in  haemorrhage. — Firstly,  where  that 
deficiency  is  due  to  actual  haemorrhage,  the  emptiness  of 
the  vascular  system  is  easily  understood,  although  I  am  not 
so  sure  that  the  effect  of  this  emptiness  upon  the  heart,  lungs, 
and  liver  is  generally  recognised. 

The  following  is  a  good  illustrative  case  : — 

Case  IV. — Nurse  A.,  suffering  from  enteric  fever,  had  a 
sudden  severe  haemorrhage  amounting  to  some  three  pints  of 
blood  or  more.  After  the  haemorrhage,  it  was  found  that  the 
liver  dullness  was  greatly  diminished  and  that  intestinal 
resonance  was  obtainable  for  some  1|  inches  above  the 
right  costal  arch.  After  the  subcutaneous  administration  of 
saline  solution,  the  liver  dullness  increased  again  in  area, 
and  at  the  end  of  thirty-six  hours  was  back  again  at  the 
costal  arch. 

No  more  need  be  said  on  this  subject,  and  the  examination 
of  almost  any  case  of  severe  haemorrhage  will  show  the  diminu- 
tion in  the  liver  dullness  here  described. 

2.  It  wiU  be  easily  understood  that  a  similar  state  of 
things  will  result  from  the  dehydration  of  the  body  which 
results  from  profuse  diarrhoea  and  vomiting. 

3.  In  some  cases  of  anaemia,  the  condition  of  liver  and 
diaphragm  point  to  the  fact  that  the  total  volume  of  the  blood 
is  lessened  and  that  the  vascular  system  is  badly  filled ;  but 
the  relationship  of  high  diaphragm  and  smallness  of  the  liver 
to  anaemia  is  somewhat  complicated,  and  I  have  not  yet  had 
the  opportunity  of  working  out  the  solution  of  the  problem 
thus  presented. 

4.  In  compensatory  diminution  of  the  volume  of  the  blood. 
— In  yet  another  gi'oup  of  cases  where  smallness  of  the  liver 
dullness  is  well  marked  and  is  sometimes  accompanied  by 
high  diaphragm  as  well,  it  seems  that  the  total  volume 
of  the  blood  in  active  circulation  has  been  cut  down  bj^ 
some  compensatory  mechanism  because  of  a  deficiency 
within  the  body  of  some  of  the  essential  constituents  of  the 
blood. 


204 


SMALL  LIVER  DULLNESS 


Small  Liver  in  Starvation,  &c. 

(a)  The  simplest  instance  of  such  a  deficiency  occurs  in 
the  case  of  a  deficiency  in  the  absorj^tion  of  ordinary  nutritive 
materials,  proteids,  &c.,  such  as  occurs  in  simple  starvation. 

The  effect  of  starvation  can  easily  be  observed,  clinically, 
where  cases  of  gastric  ulcer  are  fed  by  the  bowel  only.  Careful 
percussion  of  the  stomach  and  liver  in  such  a  case  will,  as  a 
rule,  show  that  day  by  day  the  level  of  the  gastric  resonance 


Small  Liver  Dullness  due  to  Malnutrition 


Fig.  54.— Case  V. 

A  case  of  gastric  ulcer,  showing 
small  liver  dullness  after  six  days' 
rectal  feeding. 


Fig.  55.-CASE  VI. 

Very  small  liver  dullness  and  very 
high  diaphragm  in  malnutrition  from 
pyloric  narrowing. 

The  dotted  line  shows  the  edge  of 
the  aVjsolute  liver  dullness  when  the 
patient  sits  up  and  leans  forward. 


rises  (showing  a  rise  of  the  diaphragm),  and  the  area  of  liver 
dullness  diminishes  owing  to  the  increasing  emptiness  of  its 
blood-vessels.  A  series  of  such  observations  is  given  in 
Essay  II,  at  p.  170,  where  six  figures  are  given — namely,  figs. 
25-30,  showing  the  changes  which  took  place  on  diminishing 
and  on  increasing  the  amount  of  food  given. 

I  here  reproduce  fig.  26,  showing  the  extreme  reached 
after  six  days  of  rectal  feeding  {vide  fig.  54). 

A  similar  change  may  also  be  sometimes  seen  in  enteric 
fever,  where  a  patient  is  sometimes  brought  very  low  owing 


IN  SMALL  BLOOD  VOLUME  205 

to  the  interference  with  intestinal  absorption  which  results 
from  the  inflammatory  swelhng  of  the  mesenteric  lymphatic 
glands. 

In  this  group  of  cases  the  careful  observation  of  the  size 
of  the  liver  and  the  level  of  the  diaphragm  gives  most  valuable 
information  as  to  the  degree  in  which  the  general  nutrition 
of  the  patient  is  effected. 

A  well-marked  case  of  diminution  in  the  area  of  the  liver 
dullness,  due  to  defective  nutrition,  is  the  following  (lide 
Case  VI,  fig.  55). 

W.  0.,  aged  forty-six,  had  suffered  for  very  many  years  from 
indigestion,  consisting  of  severe  pain  coming  on  a  couple  of  hours 
after  meals.  Latterly,  the  pain  had  been  so  troublesome  that 
he  had  taken  very  Httle  food,  and  he  had,  moreover,  periodic 
attacks  of  vomiting.  Examination  of  the  abdomen  showed 
that  he  was  suffering  from  pyloric  stenosis  with  compensatory 
hypertrophy  of  the  gastric  muscles  and  no  material  amount  of 
dilatation.  The  man  had  been  living  an  outdoor  life  in  South 
Australia,  and  working  hard. 

The  liver  dullness  was  extremely  small  as  he  lay  on  his 
back,  and  its  absolute  dullness  began  at  the  upper  border  of  the 
fifth  rib  in  the  right  nipple  line,  but  there  was  intestinal  reson- 
ance in  the  fifth  interspace.  The  absolute  dullness  did  not  reach 
inwards  much  beyond  the  nipple  line,  and  in  the  axilla  its  lower 
limit  was  very  much  higher  than  normal. 

In  the  middle  line  the  full  gastric  resonance  reached  up  to 
the  level  of  the  fourth  interspace,  and  there  were  only  some 
1|  inches  of  relative  dullness  separating  the  gastric  from  the 
lung  resonance. 

The  part  played  by  flaccidity  of  the  liver  in  this  case  was 
well  shown  by  the  fact  that  when  the  man  sat  up  and  leant  well 
forward,  the  liver  dullness  returned  to  its  normal  situation 
anteriorly,  and  there  was  nearly  or  quite  the  usual  area  of 
dullness  in  and  internal  to  the  nipple  line ;  but  the  liver  dullness 
disappeared  from  the  back,  and  the  intestinal  note  could  be 
got  up  as  far  as  the  lower  level  of  the  lung  resonance  about  the 
tenth  rib.  There  was  no  absolute  dullness  at  the  back,  behind 
the  mid-axillary  line  when  the  man  was  in  this  position.  There 
was  a  little  relative  dullness ;  but  over  the  greater  part  of  the  area 
usually  occupied  by  the  liver  dullness  there  was  fuU  intestinal 
resonance. 


206 


SMALL    LIVER   DULLNESS 


Small  Liver  in  Myxcedema 

{h)  The  next  group  of  cases  is  less  simple  in  their  causation 
than  the  last,  and  less  easily  understood,  but  they  form  an 
intermediate  group  between  the  last  group  and  the  next, 
which  is  more  complex  still. 

In  this  group  it  seems  as  if  the  deficiency  of  some  important 
internal  secretion  led  to  a  compensatory  hmitation  of  the 
volume  of  the  blood  in  circulation. 


Small  Liver  Dullness  in  Neurasthenia 


Fig.  56.— Case  VII. 

Small  liver  dullness  in  myxoedema. 


Fig.  57.— Case  VIII. 


Small  heart  and  liver  dullness  with  high 
diaphragm  in  neurasthenia. 


The  following  is  such  a  case  which  was  described  in  the 
last  essay,  although  the  theory  there  given  is  inadequate 
to  explain  the  chnical  picture. 

Case  VII. — The  patient  was  a  labourer  who  either  could 
not  or  would  not  work,  and  constantly  complained  of  lassitude. 
The  man  was  to  all  appearances  in  perfect  health,  suffering 
from  nothing  more  than  a  little  dyspepsia.  Careful  physical 
examination,  however,  showed  a  very  high  diaphragm  (on  the 
left  side  mainly)  and  also  a  most  marked  diminution  in  the  area 
of  the  liver  dullness,  as  is  shown  by  the  diagi-am  (fig.  38), 
which  I  here  reproduce  {vide  fig.  56). 

This  smallness  of  the  liver  dullness  and  high  gastric  reso- 
nance suggested  some  fault  in  his  cu'culation  which  would  account 


IN  SMALL  BLOOD  VOLUME  207 

for  his  weakness.  None  was,  however,  found.  In  spite  of  his 
colour  being  good,  there  was  something  in  his  appearance  and 
his  symptoms  which  suggested  myxoedema.  Thyroid  extract 
was  therefore  tried,  with  the  result  that  it  entirely  cured  him. 
I  am  sorry,  however,  that  I  did  not  take  a  second  diagram 
to  demonstrate  the  contrast. 


Small  Liver  in  Neurasthenia 

(c)  In  the  last  group  with  which  I  have  to  deal,  the  fact 
of  high  diaphragm  and  small  liver  dullness  can  be  noted  in 
association  with  certain  symptoms  of  weakness  and  incapacity 
suggesting  compensatory  diminution  in  the  volume  of  the 
blood.  Often  in  such  cases,  by  means  of  treatment  along 
general  lines,  there  are  evidences  of  improvement  in  the  circu- 
lation, with  the  retmn  of  the  liver  and  diaphragm  to  their 
normal  relationships ;  but  no  light  is  shed  upon  the  nature 
of  the  substance  which  was  presumably  deficient  in  the  blood, 
and  which  caused  a  compensatory  diminution  in  its  volume. 

It  is  especially  in  certain  cases  of  neurasthenia  that  this 
smallness  of  the  liver  can  be  found.  In  such  a  case  it  is 
presumably  some  one  of  the  substances  necessary  for  the 
proper  nutrition  of  the  nervous  system  which  is  deficient, 
and  which  under  treatment  and  rest  gradually  re-accumulates 
in  the  system  until  its  normal  percentage  is  once  more  restored. 

Case  VIII. — The  following  is  such  a  case.  Mrs.  B.,  aged 
twenty-six,  came  to  me  Feburary  1906,  some  months  after  the 
birth  of  her  first  child,  complaining  of  distressing  fancies  of 
various  kinds,  which  worried  her  much,  and  which  she  could 
not  shake  off.  They  made  her  so  self-conscious  that  she  could  not 
go  out  into  society.  She  also  had  most  troublesome  salivation. 
She  was  to  all  appearances  in  perfect  health,  and  very  well 
nom'ished,  with  no  trace  of  anaemia  or  dyspepsia  or  other  ail- 
ment. On  examining  the  liver  dullness,  it  was  found  to  be 
remarkably  small.  There  was  no  absolute  dullness  internal  to 
the  right  nipple  line,  and  the  relative  dullness  did  not  come  near 
the  costal  arch.  There  was  no  absolute  cardiac  dullness,  and  the 
relative  dullness  would  be  covered  by  a  half-crown  piece.  The 
stomach  resonance  was  up  to  the  fifth  interspace  {vide  fig.  57). 
In  spite  of  her  healthy  appearance  and  good  colour,  it  was 


208  SMALL  LIVER  DULLNESS 

therefore  probable  that  the  total  volume  of  her  blood  was  small. 
On  inquiry,  it  transpired  that  she  had  eaten  very  little  meat 
throughout  her  pregnancy,  adopting  largely  a  vegetarian  and 
fruit  diet.  It  seemed  probable  that  this  had  not  been  sufficient 
for  her,  although  its  proteid  content  seemed  fairl}^  good.  She 
was  put  on  full  meat  diet  with  a  little  thyroid  extract,  and  in 
four  weeks  her  liver  dullness  had  returned  nearly  to  the  normal 
size — the  absolute  dullness  reaching  to  the  costal  arch — and  she 
had  much  more  control  over  her  thoughts.  She  continued 
steadily  to  improve.  Here  the  size  of  the  liver  dullness  gave  the 
clue  to  the  cause  of  the  neurasthenia  and  its  treatment. 

This  smallness  of  the  hver,  with  or  without  a  high  dia- 
phragm, will  very  frequently  be  found  to  occur  associated 
with  neurasthenia. 

It  is,  in  my  opinion,  probable  that  all  cases  of  neurasthenia 
may  be  divided  into  two  classes — distinct  both  as  regards 
cause  and  treatment — by  the  presence  or  absence  of  this 
symptom. 

Enough  has  now,  I  think,  been  said  to  show  the  importance 
of  the  little-known  physical  signs  which  form  the  subject  of 
this  essay. 


Essay  IV.— ON  SOME  DIAGNOSTIC  DIFFICULTIES 
ASSOCIATED  WITH  DILATATION  OP  THE  EIGHT 
VENTEICLE  i 

For  the  purposes  of  this  essay  it  will  be  convenient  to 
divide  cases  of  dilatation  of  the  right  ventricle,  clinically,  into 
three  main  groups. 

Firstly. — Cases  where  the  tricuspid  valve  becomes  incom- 
petent, and  the  regurgitation  which  occurs  takes  place  mainly 
upwards  into  the  superior  vena  cava  and  its  branches,  thus 
giving  rise  to  pulsation  in  the  veins  of  the  neck. 

Secondly. — Cases  where  the  tricuspid  incompetence  mainly 
takes  effect  downwards  into  the  hver,  and  there  is  no  evidence 
of  regurgitation  of  blood  upwards  into  the  veins  of  the  neck. 

Thirdly. — Cases  Avhere  tricuspid  regurgitation  does  not 
necessarily  play  an  important  part  in  the  chnical  features  of 
the  case,  but  where  the  dilatation  mainly  involves  the  upper 
part  of  the  anterior  wall  of  the  right  ventricle — i.e.,  the 
so-called  conus  arteriosus. 

The  first  two  of  these  three  types  most  commonly  occur 
secondarily  to  valvular  disease,  whereas  the  best  marked  cases 
of  the  third  type  are  seen  in  the  dyspnoea  of  anaemia  and 
cardiac  overstrain. 

Although  each  of  these  types  of  right  ventricular  failure  often 
occurs  more  or  less  independently  of  the  others,  no  hard-and- 
fast  line  is  to  be  drawn,  for  they  may  each  or  all  occur  simulta- 
neously or  successively  in  any  particular  case  of  cardiac  failure. 
As  a  general  rule,  the  third  type  of  right  ventricular  failure  is 
relatively  more  common  in  youth  and  adolescence  than  it  is 
later  in  life. 

Ishall  only  refer  briefly  to  the  second  of  these  three  gioups, 
and  shall  therefore  take  it  up  first.  I  shall  then  consider 
the  third  group,  and  shall  take  up  the  first  group  last. 

^  See  Birmivrjham  Medical  Review,  June  1900. 

209  V 


210         DILATATION  OF  THE  EIGHT  VENTRICLE 

In  the  second  group  the  tricuspid  reflux  mainly  expends 
its  force  in  dilating  the  lower  and  less  muscular  portion  of  the 
right  auricle  and  in  distending  the  liver. 

In  these  cases  it  seems  as  if  the  regurgitating  blood  were 
prevented  from  passing  upwards  into  the  veins  of  the  neck 
by  the  satisfactory  muscular  tone  of  the  right  auricle  and  of 
the  veins,  and  that,  as  a  consequence,  the  lower  part  of  the 
auricle  and  the  liver  had  to  bear  the  brunt  of  the  regurgitation. 
It  is  possible,  however,  that  the  reverse  of  this  is  the  true 
sequence — namely,  that  the  veins  of  the  neck  escape  because 
the  Eustachian  valve  gives  way  early  in  the  case. 

Clinically,  it  is  by  no  means  uncommon  to  see  cases  where 
the  liver  is  so  enlarged  that  its  lower  edge  is  at  or  below  the 
level  of  the  umbilicus,  and  where  the  organ  can  be  felt  to 
pulsate  from  distension  at  each  beat  of  the  heart,  but  yet  no 
pulsation  is  observable  in  the  veins  of  the  neck.  Two  such 
cases  I  have  seen  within  the  last  week  or  two,  and  I  have  the 
notes  of  an  extreme  case  where  there  was  an  aneurysmal 
dilatation  of  the  lower  part  of  the  auricle  and  of  the  part  of  the 
inferior  vena  cava  above  the  diaphragm.  In  this  case  the 
cavity  of  the  right  auricle  held  570  c.c,  or  exactly  20  ounces, 
when  moderately  distended  ;  and  of  this  about  8  ounces,  as 
far  as  could  be  estimated,  was  the  content  of  the  aneurismal 
dilatation  above  referred  to.  The  physical  signs  in  these 
cases  do  not  leave  much  room  for  doubt  as  to  the  diagnosis, 
and  I  shall  therefore  pass  on  to  the  other  two  groups. 

I  shall  now  speak  of  difficulties  in  diagnosis  included  in 
the  third  of  my  three  groups — ^namely,  where  the  right  ventricle 
dilates  upwards  in  the  manner  so  fully  described  by  the  late 
Dr.Foxwell  in  his  Paper  on '  The  Heart  in  Anaemia  and  Debility,' 
in  the  Lancet  for  the  year  1891,  in  'Essays  in  Heart  and  Lung 
Disease,'  and  most  recently  in  the  Bradshaw  Lecture,  1899. 

In  this  type  of  dilatation,  the  following  difficulties  may 
arise : — 

1.  The  right  ventricular  pulsation,  which  is  visible  and  pal- 
pable in  the  second  left  interspace,  may  be  mistaken  for  that  of 
an  aneurysm  of  the  transverse  arch  of  the  aorta,  or  vice  versa. 
Cases  are,  I  believe,  on  record  when  the  former  error  was 
made,  and  I  shall  recount  later  on  a  case  where  it  was  by  no 


DIAGNOSTIC  DIFFICULTIES  211 

means  easy  to  distinguish  an  aneurysm  of  the  aorta  fi-om  a 
dilatation  of  the  right  ventricle. 

2.  Another  difficulty,  to  which  I  shall  refer,  is  that  which 
sometimes  occurs  in  distinguishing  the  systohc  pulmonary 
murmur,  which  results  from  this  type  of  dilatation,  from  a 
murmur  of  aortic  origin. 

Before  taking  up  these  two  points  it  will  perhaps  be  well  to 
say  a  few  words  as  to  this  upward  dilatation  of  the  ventricle. 
In  this  type  of  dilatation,  as  I  have  previously  stated,  tricuspid 
regurgitation  does  not  play  an  essential  part,  and  the  tricuspid 
valves  may  be,  and  I  beUeve  often  are,  quite  competent.  This 
upward  dilatation  seems  to  result  when  the  work  to  be  done 
by  the  contracting  ventricle  exceeds  the  resisting  power  of 
the  weakest  part  of  its  wall.  ^ATien  this  state  of  matters  occm-s, 
the  ventricle  wall  -^ill  bulge  at  the  weak  spot.  This  may  be 
well  illustrated  by  gi-asping  a  partly  filled  rubber  toy  balloon. 
When  this  is  done,  the  portion  outside  the  hand  vdU.  be  made 
to  bulge  by  the  compression  of  the  part  ^-ithin  the  giasp  of 
the  hand. 

In  the  case  of  the  right  ventricle,  the  lower  part  of  the 
ventricle  is  the  strongest.  "WTien  the  resistance  to  be  overcome 
in  the  pulmonary  artery  exceeds  the  resisting  power  of  the 
thin  portion  of  the  anterior  wall  which  lies  just  below  the 
pulmonary  valves,  this  weaker  part  will  be  made  to  bulge 
upwards  and  forwards  with  each  contraction  of  the  ventricle. 
This  upward  bulging  is  often  so  considerable  that  the  pul- 
monary valves  come  to  he  under  the  second  rib  or  even  higher, 
and  in  such  cases  the  systoUc  pulsation  of  the  right  ventricle 
may  be  seen  and  felt  in  the  second  left  interspace.  This 
pulsation  may  be  mistaken  for  that  of  an  anemysm,  or  vice 
versa. 

Without  going  at  all  fuUy  into  all  physical  signs  of  this 
dilatation,  I  must  nevertheless  dwell  for  a  short  time  on  those 
which  bear  upon  my  present  subject.     They  are  : — 

(a)  Increase  of  the  heart  upwards,  giving  rise  to  a  consider- 
able amount  of  relative  cardiac  dullness  in  the  second  left  inter- 
space and  sometimes  to  absolute  dullness  also.  In  addition, 
there  is  considerable  increase  of  the  cardiac  dullness  in  the  third 
left  interspace. 

p2 


212  DILATATION  OF  THE  EIGHT  VENTRICLE 

(b)  Systolic  pulsation  in  the  second  left  interspace. 

(c)  A  well-marked  systolic  murmur  heard  over  the  area 
of  dullness  above  mentioned  ;  and  in  extreme  cases  a  well- 
marked  systolic  thrill.  The  point  of  maximum  intensity 
of  the  murmur  is  not  infrequently  an  inch  or  more  away 
from  the  sternum,  just  as  might  be  expected  in  a  case  of 
aneurysm. 

(d)  There  is  also,  sometimes,  a  considerable  amount  of 
tenderness  and  of  pain  on  exertion  over  the  pulsating  area. 

(e)  Some  patients  also  complain  of  a  choking  feeling  in  the 
throat — as  if  some  food  had  stuck  in  the  throat  opposite  the 
upper  end  of  the  sternum.  This,  too,  is  a  sjnuptom  of  aneurysm 
of  the  transverse  arch  of  the  aorta. 

To  give  an  instance  :  I  have  seen  a  young  man  about  thirty, 
who,  when  convalescent  from  an  attack  of  pneumonia,  ran 
nearly  half  a  mile  to  escape  a  threatened  shower  of  rain.  On 
reaching  his  destination,  he  was  much  out  of  breath,  and  was 
alarmed  somewhat  at  remaining  so  ;  he  also  had  rather  a 
sharp  pain  above  the  left  nipple.  When  I  examined  him 
shortly  afterwards,  I  found  there  was  systolic  cardiac  pulsation 
in  the  second  left  interspace  with  a  systolic  murmm-.  There 
was  considerable  tenderness  in  the  second  left  interspace  on 
percussion,  and  the  patient  complained  of  a  dull  aching 
pain  in  the  same  situation,  which  was  worse  on  exertion, 
and  also  of  a  sensation  in  the  throat— such  as  I  have  just 
referred  to. 

In  tliis  case,  I  had  no  difficulty  in  diagnosing  acute  dilatation 
of  the  right  ventricle  from  overstrain ;  but  had  the  case  been 
rather  more  severe  it  would  not  have  been  so  easy  to  come  to 
a  diagnosis.  I  have  often  seen  similar  symptoms  in  apparently 
healthy  young  men  as  a  result  of  rowing  or  other  form  of 
excessive  muscular  exertion. 

Although  I  have  not  yet  seen  a  case  of  dilatation  of  the 
right  ventricle  where  I  could  not  on  careful  examination 
certainly  exclude  aneurysm  of  the  aorta,  I  have  seen  a  case 
of  aneurysm  of  the  aorta  in  a  young  woman  where,  on  my 
first  examination,  I  found  it  impossible  to  diagnose  the  condition 
from  dilatation  of  the  right  ventricle.  A  second  examination, 
however,  after  the  patient  had  been  taking  somewhat  sharp 


DIAGNOSTIC  DIFFICULTIES  213 

exercise,  sufficed  to  clear  up  the  diagnosis.  But  even  after 
I  was  convinced  of  the  presence  of  an  aneurysm,  the  symptoms 
and  physical  signs  were  at  times  so  exactly  like  those  of 
dilatation  of  the  right  ventricle  that  I  was  once  or  twice  almost 
tempted  to  doubt  my  own  diagnosis. 

Both  before  and  aiter  the  period  when  the  patient  was 
under  my  care,  I  beUeve  that  she  consulted  several  other 
physicians,  and  if  I  am  correctly  informed  there  was  a 
strildng  lack  of  unanimity  in  the  diagnosis  at  wliich  they 
arrived.  Fuller  particulars  of  this  case  will  doubtless  therefore 
be  interesting. 

The  first  case  I  refer  to  is  that  of  Mrs.  P.,  whom  I  first  saw  in 
October  1897.  She  was  then  aged  thirty.  She  was  complain- 
ing of  an  intermittent  pain  in  the  left  pectoral  region,  which  was 
increased,  or  brought  on,  by  exertion  and  sometimes  radiated 
down  the  left  arm.  She  had  had  the  pain  more  or  less  for  two 
or  three  years.  Earlier  in  life,  her  occupation  had  involved  a 
certain  amount  of  hard  work  and  occasional  muscular  strain. 
Since  her  marriage,  in  1893,  she  had  lived  an  easy  life.  She 
began  to  suffer  from  ill-health  soon  after  her  marriage,  but  she 
dates  her  present  symptoms  from  a  severe  attack  of  plemisy  in 
1895,  two  and  a  half  years  prior  to  the  time  when  I  first  saw  her. 
For  the  last  eighteen  months  she  had  been  much  the  same  as 
when  I  saw  her.  She  had  a  miscarriage  soo^i  after  recovery 
from  the  pleurisj^  but  there  was  no  history  of  syphilis  discover- 
able. She  was  well  nourished  and  of  a  healthy  appearance, 
and  not  specially  ansemic.  The  chief  complaint  was  of  the 
pain  in  her  left  pectoral  region.  It  was  not  constant.  It 
would  be  troublesome  for  two  or  three  daj'S  at  a  time  and  then 
disappear  for  two  or  three  weeks.  It  was  sometimes  bad  at 
night,  and  came  and  went  like  neuralgia.  It  was,  however, 
increased  by  exertion,  and  was  accompanied  I.)}'  slight  dyspnoea 
and  some  palpitation.  As  to  the  situation  of  the  pain  it 
would  usually  commence  about  the  left  breast  and  shoot 
through  to  the  back  and  also  down  the  left  arm  and  some- 
times to  the  right  arm  also.  She  had  been  unable  to  do  any 
work  for  some  months  on  account  of  the  pain  being  brought 
on  easily  by  movements  of  the  arms.  She  also  complained  of 
a  sensation  of  a  lump  in  the  throat  when  she  was  excited. 

As  to  the  Physical  Examination  of  the  Chest. — On  inspection 
there  was  slight  diffuse  pulsation  visible  in  the  second,  third,  and 


214         DILATATION  OF  THE  RIGHT  VENTRICLE 

fourth  left  interspaces.  The  apex  was  under  the  fifth  rib,  a 
little  external  to  the  nipple  line.  The  cardiac  dullness  extended 
to  the  second  rib,  being  nearly  absolute  below  the  level  of  the 
fourth  rib.  There  was  no  pulsation  in  the  fifth  interspace.  To 
the  right  the  heart  dullness  did  not  extend  beyond  the  left  edge 
of  the  sternum.  There  was  no  murmur  audible  at  the  apex  or 
in  the  axilla.  There  was,  however,  a  loud  systolic  murmur  at 
the  base  of  the  heart,  heard  best  over  the  second  left  interspace, 
2|  inches  from  sternum.  This  systolic  murmur  was  audible 
over  an  area  about  the  size  of  the  palm  of  the  hand,  and  in  spite 
of  its  extreme  loudness  it  was  not  at  all  well  conducted  into 
the  vessels  of  the  neck.  The  murmur  was,  however,  audible 
posteriorly.  It  was  loudest  about  the  middle  third  of  the 
interscapular  area  on  both  sides  of  the  spine.  It  was  less  loud 
at  the  angle  of  the  left  scapula,  and  was  not  audible  as  far 
forward  as  the  left  axilla. 

I  felt  unable  to  arrive  at  a  definite  diagnosis  at  this  visit. 
The  physical  signs  and  symptoms  would  do  for  either  aneurysm 
of  the  transverse  arch  of  the  aorta  or  for  upward  dilatation  of 
the  right  ventricle  from  overstrain.  The  severity  of  the  pain, 
the  duration  of  the  symptoms,  and  the  conduction  of  the 
murmur  were  certainly  suggestive  of  aneurysm.  The  pulsation 
was,  however,  of  the  ill-defined  type  so  characteristic  of  right 
ventricular  pulsation  as  seen  in  the  second  left  interspace.  I 
omitted  on  this  occasion  to  make  the  patient  take  a  little  active 
exertion,  or  I  should  have  lessened  my  uncertainty.  On  a 
subsequent  visit,  after  a  little  brisk  walking,  the  pulsation  in  the 
second  left  interspace  became  much  more  evident  ;  it  was  now 
strong  and  arterial  in  type,  and  from  this  and  other  symptoms 
I  had  no  hesitation  in  diagnosing  aneurism  of  the  transverse 
part  of  the  arch  of  the  aorta. 

By  my  advice  she  took  to  her  bed,  and  had  more  than  a  year 
of  absolute  rest.  After  this,  having  heard  something  about  the 
X-rays,  she  became  anxious  to  be  examined  by  their  aid,  and 
this  was  done  by  Mr.  Hall-Edwards  in  my  presence.  There  was 
clearly  a  dark  shadow  in  the  region  of  the  suspected  aneurysm, 
which  was  distinct  from  the  heart,  and  which  pulsated.  This 
left  no  room  for  doubt  as  to  the  diagnosis.  As  the  patient  was 
now  fairly  free  from  pain  on  exertion  and  seemed  much  better, 
she  began  to  get  about  rather  more,  but  was  still  very  careful. 
She  seemed  to  be  getting  on  fairly  well  till,  one  day,  as  the 
result  of  some  slight  exertion,  the  aneurysm  ruptured  into  a 
bronchus,  and  she  died  suddenly  of  haemoptysis. 


•      DIAGNOSTIC  DIFFICULTIES  215 

The  points  of  diagnostic  importance  in  these  cases  seem  to 
me  to  be  as  follows  : — 

(a)  The  character  of  the  impulse  in  the  second  space. 

(&)  Non-conduction  of  the  murmur  to  the  neck  to  the 
extent  wliich  would  be  the  case  if  the  murmur  were  a  pulmonary- 
artery  murmur. 

(c)  Its  loudness  posteriorly  in  the  interscapular  area. 

(d)  The  severity  of  the  attacks  of  pain. 

(e)  A  separation  of  the  aneurysmal  dullness  from  tho 
cardiac  dullness.     This  was  not  present  in  this  case. 

(/)  Examination  by  the  Eontgen  rays. 

{g)  In  such  a  case  as  this  the  cardiograph  is  of  great  value 
in  clearing  up  the  diagnosis. 

I  need  hardly  point  out  that  the  gi-eat  difference  between 
both  the  prognosis  and  treatment  of  aneurysm  and  dilatation 
of  the  right  ventricle  makes  an  error  in  diagnosis  a  serious 
one  in  such  a  case. 

I  now  come  to  my  second  subheading — namely,  the  diffi- 
culty which  may  sometimes  arise  in  distinguishing  the  systolic 
murmur  which  accompanies  this  type  of  dilatation  of  the 
right  ventricle  from  a  systohc  murmur  of  aortic  origin.  In  the 
slighter  cases  of  upward  dilatation  of  the  right  ventricle,  such 
as  are  ordinarily  seen  in  the  dyspncea  of  anaemia,  this  diffi- 
culty does  not  arise,  because  the  area  over  which  the  murmur 
is  audible  is  hmited  to  the  left  side  of  the  sternum  with  its 
point  of  maximum  intensity  in  the  second  left  interspace. 
In  the  more  severe  cases  of  dilatation  which  occur  whei^  the 
anaemia  is  very  considerable  or  where  the  overstrain  has  been 
great,  the  pulmonary  artery  mm-mur  may  be  propagated  into 
the  aorta  and  its  branches.  The  pulmonary  artery  murmur 
may  thus  resemble  an  aortic  sj^stohc  murmur.  I  have  notes  of 
many  cases  where  I  have  heard  the  pulmonary  artery  murmur 
conducted  into  the  subclavian  arteries,  carotids,  and  even 
into  the  axillary  arteries. 

A  glance  at  the  relationship  of  the  pulmonary  artery  to 
the  aorta  ^411,  I  think,  show  how  this  conduction  is  brought 
about.  The  pulmonary  artery  murmur  is  produced  in  a 
dilated  pulmonary  artery.  The  dilatation  is  brought  about 
as    follows.     The   upward    dilatation   of   the   right    ventricle 


216         DILATATION  OF  THE  RIGHT  VENTRICLE 

naturally  carries  the  pulmonary  valves  up  with  it.  As  the 
normal  course  of  the  pulmonary  artery  is  upwards  its  course 
must  be  shortened  by  this  upward  movement  of  its  origin. 
This  shortening  must  cause  relaxation  of  its  elastic  walls, 
and  this  relaxation  must  admit  of  an  aneurysmal  bulging  of 
the  walls  under  the  systolic  blood  pressure. 

Considering  how  close  the  aorta  hes  above  the  pulmonary 
artery,  normally,  any  upward  movement  of  dilatation  of  the 
latter  must  bring  it  into  very  close  contact  with  the  aorta. 
This  contact  is  so  close  that  the  murmur  vibrations  of  the  blood 
in  the  pulmonary  artery  mil  be  able  to  spread  through  to  the 
blood  in  the  aorta  l^y  contiguity  of  tissue.  Hence  the  murmur 
may  become  audible  in  the  arteries,  and  does  on  superficial 
examination  simulate  an  aortic  murmur. 

When  the  possibility  of  an  occasional  arterial  conduction 
of  the  pulmonary  systolic  murmur  is  once  recognised  its 
diagnosis  from  an  aortic  systolic  murmur  is  as  a  rule  compara- 
tively easy.     The  following  are  the  chief  points  to  be  noted  : — 

(a)  The  point  of  maximum  intensity  of  the  murmur  is 
in  the  second  left  interspace,  often  half  an  inch  or  more  away 
from  the  sternum. 

(b)  The  mm-mur  is  less  loud  in  the  arteries  of  the  neck  than 
it  is  in  the  second  left  interspace.  Tliis  is  perhaps  the  most 
important  diagnostic  sign.  If  the  murmur  be  produced  at 
the  aortic  orifice  it  must  be  heard  at  least  as  loudly  over  the 
carotid  arteries  as  over  the  sternum  ;  for  if  the  blood  in  the  aortic 
orifice  were  vibrating  sufiiciently  strongly  to  produce  a  murmur 
wliich  is  audible  through  the  sternum  and  lungs,  it  is  hardly 
conceivable  that  the  vibrations  should  have  sensibly  diminished 
in  loudness  during  the  verj^  small  fraction  of  a  second  which  it 
takes  for  the  blood  to  reach  the  carotid  arteries,  where  only  the 
skin  and  a  little  muscular  tissue  intervene  between  the  vibrating 
blood  and  the  stethoscope. 

(c)  Another  fact  wliich  will  sometimes  afford  assistance 
is  that  the  pulmonary  artery  murmur  is,  I  think,  usually  better 
conducted  to  the  left  carotid  and  subclavian  than  to  the  right 
(possibly,  because  the  point  where  the  pulmonary  artery  comes 
most  closely  in  contact  ^^^th  the  aorta  is  higher  than  the  point 
where  the  innominate  artery  is  given  off).     Not  infrequently, 


DIAGNOSTIC  DIFFICULTIES  217 

however,  there  are  other  systolic  murmurs  present  in  the  neck 
which  will  prevent  this  observation  from  being  made.  This  is 
especially  the  case  with  the  systohc  mmmm*,  of  which  I  shall 
speak  later,  wMch  originates  in  the  superior  vena  cava,  and 
which  is  apt  to  occur  in  those  cases  of  anaemic  dilatation  of 
the  heart.  It  is  heard  well  to  the  right  of  the  sternum,  and  in  the 
vessels  on  the  right  side  of  the  neck  better  than  on  the  left  side. 
When  it  occurs  with  the  pulmonar}^  systolic  murmur  it  will 
render  the  diagnosis  from  aortic  disease  a  little  less  easy. 

(d)  Other  signs  of  dilatation  of  the  right  ventricle  will  be 
present,  such  as  increase  of  the  cardiac  dullness  upwards.  More- 
over, in  cases  w-here  the  pulmonary  systolic  murmur  is  loud 
enough  to  be  conducted  well  into  the  arteries  there  will  in 
all  probabihty  be  the  typical  right  ventricular  pulsation  in 
the  second  left  interspace,  also  a  degree  of  anaemia  will  be 
present  that  will  be  suggestive  of  the  '  haemic  '  origin  of  the 
mm'mur. 

Difficulties  of  Diagnosis  in  Connection  with  the 
Murmurs  due  to  Tricuspid  Eegurgitation 

The  murmurs  due  to  tricuspid  regurgitation  may  give  rise 
to  difticulties  in  various  ways ;  but  in  order  to  get  a  clear 
idea  of  them  it  is  well  to  remember  that  the  stream  of 
blood  on  regurgitation  through  the  tricuspid  valve  may  give 
rise  to  a  systolic  murmur  at  three  different  points  during  its 
course  from  the  right  ventricle  to  the  vems  of  the  neck.  Firstly, 
at  the  tricuspid  valve  itself  ;  secondly,  at  the  point  where 
a  distended  superior  vena  cava  wiU  be  constricted  on  passing 
through  the  pericardium,  owing  to  the  non-dilatation  of  the 
ring  which  receives  support  from  that  structure  ;  and  thirdly, 
a  murmm-  ma}^  much  more  rarely  arise  at  the  valves  in  the 
veins  themselves,  when  these  first  give  way  in  the  face  of  the 
tricuspid  regurgitation. 

The  True  Tricuspid  Murmur. — The  main  difficulty  in 
the  diagnosis  of  this  murmur  is  to  decide  whether  a  murmur 
heard  to  the  left  of  the  sternum  is  really  of  tricuspid  origin. 
In  cases  where  the  left  ventricle  is  but  little  enlarged  and  the 


218         DILATATION  OF  THE  RIGHT  VENTRICLE 

greater  part  of  the  front  of  the  heart  is  occupied  by  the  right 
ventricle,  a  tricuspid  may  resemble  a  mitral  murmur  ;  but  if 
the  direction  of  conduction  be  noted,  no  error  need  be  made, 
for  if  there  is  a  tricuspid  murmur  it  will  be  conducted  down 
and  to  the  right  as  clearly  as  is  the  right  ventricle  first  sound  ; 
whereas  if  the  murmur  be  of  mitral  origin  this  will  not  be  the 
case.  The  hearing  of  a  first  sound  over  the  liver  more  free  from 
murmur  than  is  the  case  with  the  first  sound  heard  just  to  the 
left  of  the  sternum  is  strong  evidence  against  the  presence  of  a 
tricuspid  murmur,  and  a  first  sound  that  gradually  gets  more 
free  from  murmur  on  listening  towards  the  axilla  is  strong 
evidence  against  the  presence  of  a  mitral  murmur. 

As  has  already  been  said,  this  tricuspid  murmur  does  not 
occur  in  all  cases  of  tricuspid  regurgitation.  The  structure 
of  the  valve  is  such  that  leakage  very  often  occurs  without  the 
production  of  a  murmur. 

Superior  Vena  Cava  Murmur.  —  The  second  point  at 
which  a  murmur  can  arise  is  at  the  place  in  the  superior  vena 
cava,  where  its  walls  are  strengthened  on  its  passage  through 
the  pericardium  by  the  fibrous  support  given  by  that  structure. 
When  the  vein  is  over-distended  by  the  blood  which  is 
regurgitating  through  the  tricuspid  valve,  this  part  dilates 
to  a  less  extent  than  the  rest,  and  a  murmur  is  produced  by 
the  constriction  thus  caused. 

This  murmur  may  well  be  called  the  superior  vena  cava 
murmur. 

Its  characters  closely  resemble  those  of  the  aortic  systolic 
murmur,  and  the  incautious  observer  may  very  readily 
mistake  the  one  for  the  other.  The  diagnostic  points  are, 
however,  clearly  marked  if  they  are  looked  for.  They  are, 
firstly,  the  point  of  maximum  loudness  :  this  is  lower  in  the 
superior  vena  cava  murmur  than  in  the  aortic  systolic.  The 
venous  murmur  is  usually  as  well  heard  in  the  third  as  in  the 
second  interspace,  and  sometimes  in  the  fourth  also,  whereas 
the  aortic  murmur  is  not  heard  as  low  as  this. 

Secondly,  the  nature  of  the  vessel  up  which  the  murmur 
is  conducted.  It  is  not  always  as  easy  to  determine  this  as 
might  be  supposed,   because  of  the  close  proximity  of  the 


DIAC4N0STIC  DIFFICULTIES  219 

veins  and  arteries.  The  character  of  the  pulsation  is  often 
a  useful  guide,  being  weaker  and  more  fluttering  in  the  veins, 
stronger  and  more  even  in  the  arteries.  And  also,  where  the 
tricuspid  regurgitation  is  not  very  extreme,  the  murmur  and 
the  thrill  which  may  accompany  it  may  often  be  observed 
to  stop  short  suddenly  in  a  manner  suggestive  of  the 
regurgitation  being  arrested  by  competent  valves  in  the  vein. 

Where  the  regurgitation  is  great  and  the  valves  are  incom- 
petent, the  diagnosis  is  more  difficult ;  but  with  care  the  arterial 
pulsation  can  be  distinguished  from  the  venous,  and  the  absence 
of  thrill  and  murmur  in  the  arteries,  together  with  their  presence 
in  the  veins,  will  make  the  diagnosis  clear. 

Another  point  that  often  helps  to  differentiate  these  two 
murmurs  is  that  the  aortic  murmur  is  as  a  rule  better  conducted 
along  the  line  of  the  subclavian  artery  than  the  venous  murmur 
is  along  the  subclavian  vein,  owing  to  the  presence  of  the 
venous  valves. 

Tliird]}^  the  relative  loudness  of  the  mui'mur  in  the  neck, 
as  compared  with  its  loudness  in  the  second  right  interspace, 
may  prove  of  service  for  diagnosis.  In  the  case  of  the  aorta, 
the  loudness  in  the  neck  is  always  equal  or  nearly  equal  to 
its  loudness  over  the  second  rib  or  interspace. 

In  the  case  of  the  murmur  of  tricuspid  origin,  its  loudness 
in  the  neck  depends  upon  the  degree  to  which  the  valves  in 
the  veins  have  given  way.  If  there  be  free  regurgitation  up 
the  veins,  the  murmur  may  be  as  well  conducted — at  all  events 
for  a  short  distance — as  the  aortic  murmur  is.  As  a  rule, 
however,  this  is  not  the  case,  and  the  conduction  is  not  loud. 

Fourthh',  another  important  diagnostic  sign  is  the 
relationship  between  the  loudness  of  the  first  sound  and  the 
murmur  as  heard  in  the  arteries  of  the  neck.  If,  as  in  the  last 
case  referred  to,  the  first  sound  of  the  heart  can  be  heard 
over  the  arteries  in  the  neck,  while  the  murmur  is  heard  faintly 
or  not  at  all,  it  is  strong  evidence  against  the  murmur  being 
of  aortic  origin. 

MuKMUR  Produced  at  the  Venous  Valves. — The  third 
point  at  which  a  murmur  may  be  caused  by  tricuspid 
regurgitation  is  at  one  or  other  of  the  valves  which  limit  the 
auriculo-venous  reservoir.     Little  need  be  said  on  this  point,  as 


220        DILATATION  OF  THE  RIGHT  VENTRICLE 

it  is  not  very  common  for  a  murmur  to  arise  at  these  valves, 
and  when  such  a  murmur  is  caused,  the  diagnosis  is  not  difficult, 
and  it  is  not  likely  that  any  one  who  recognises  the  possibihty 
of  such  a  murmur  occurring  would  be  misled  by  it.  Such  a 
murmur  may  occur  at  the  valves  guarding  the  entrance  of 
the  external  jugular  into  the  subclavian,  or  those  at  the  lower 
end  of  the  internal  jugular.  A  case  of  this  latter  nature  is 
recorded  at  p.  291. 

Sounds  Arising  in  the  Venous  Valves. — Another  physical 
sign  of  some  interest,  but  of  no  great  practical  importance, 
is  a  sound  produced  in  the  subclavian  or  innominate  veins 
by  the  forcible  closure  of  their  valves  in  cases  of  well-marked 
tricuspid  regurgitation.  These  valve  sounds  are  not  often 
heard,  and  may  cause  some  uncertainty  when  they  are,  because 
of  their  occurrence  in  the  short  pause  of  the  heart  shortly 
after  the  first  sound  and  tow^ards  the  end  of  the  tricuspid 
systolic  murmur — if  there  be  one  present.  More  than  once,  I 
have  been  able  to  observe  that,  with  increasing  tricuspid  re- 
gurgitation, the  somid  of  valve  closure  gave  place  to  a  murmur 
produced  in  the  vein  ;  or,  on  the  contrary,  as  the  patient 
improved,  I  have  observed  a  late  systolic  murmur — which 
from  its  situation  I  had  recognised  as  arising  in  a  vein — 
disappear,  and  its  place  taken  by  the  sharp  sound  due  to  the 
closure  of  the  venous  valves.  The  first  time  I  recognised 
this  latter  phenomenon  w'as  in  a  case  of  severe  aortic  regurgi- 
tation with  a  large  amount  of  tricuspid  regurgitation.  On 
admission  to  hospital  there  was  a  loud  late  systolic  murmur 
audible  just  above  the  clavicle  on  both  sides  and  of  rather 
a  more  hissing  character  than  cardiac  murmurs  usually 
are.  In  a  few  days  the  murmur  on  the  left  side  of  the  neck 
was  no  longer  audible,  but  the  sharp  sound  of  valve  closure 
was  heard  instead,  and  then  a  few  days  later,  the  one  on 
the  right  side  of  the  neck  disappeared  in  the  same  way.  I 
have  not  infrequently  been  able  to  demonstrate  this  sound  of 
valve  closure  in  cases  of  tricuspid  regurgitation. 

The  following  cases  illustrate  some  of  the  points  just  dealt 
with  : — 

In  the  following  case,  it  was  not  at  all  easy  to  exclude  the 
existence  of  an  aortic  systolic  murmur  in  addition  to  the  tricuspid 


DIAGNOSTIC  DIFFICULTIES  221 

murmui',  wliich  was  evidently  present.  M.  T.,  aged  sixty-six, 
was  admitted  to  hospital  suffering  from  bronchitis  and  dyspncBa, 
and  some  oedema  of  the  ankles.  The  arteries  were  atheroma- 
tous and  the  arcus  senihs  well  marked.  The  apex  beat  was  much 
displaced  downwards  and  outwards,  being  in  the  sixth  inter- 
space nearly  in  the  anterior  axillary  line,  5^  inches  from  the 
sternum.  This  was  seemingly  due  to  displacement  of  the  heart 
and  not  hypertrophy,  because  there  was  almost  no  cardiac 
dullness  near  the  apex  beat,  and  the  resonance  of  the  stomach 
met  that  of  the  lung  in,  and  just  external  to,  the  nipple  line 
— ^i.e.,  between  the  apex  beat  and  the  rest  of  the  cardiac  dullness. 
Internal  to  the  nipple  line  there  was  a  Httle  relative  cardiac 
dullness  near  the  left  edge  of  the  sternum,  and  over  this  dull  area 
there  was  a  loud  systolic  murmur,  certainly  of  tricuspid  origin. 
It  was  conducted  upwards,  and  was  well  heard  to  the  right  of 
the  sternum  and  into  the  vessels  of  the  neck.  It  was  particu- 
larly well  heard  over  a  vessel  which  could  be  felt  strongly  pul- 
sating nearly  half-way  along  each  clavicle.  The  pulsation  was 
strong  and  the  vessel  felt  just  like  an  artery.  On  careful  palpa- 
tion, however,  the  carotid  could  be  felt  internal  to  it,  and  the 
murmur  was  not  heard  in  the  carotid,  and,  moreover,  the 
pulsation  in  the  previously  mentioned  vessel  stopped  short 
suddenly  some  little  distance  up  the  vessel,  in  a  manner  very 
suggestive  of  the  presence  of  valves  checking  the  regurgitation 
up  a  vein. 

In  this  case,  the  diagnosis  of  the  presence  or  absence  of 
aortic  disease  practically  turned  upon  the  question  as  to 
the  nature  of  the  vessel  in  which  the  murmur  was  heard,  and 
it  required  a  careful  examination  to  arrive  at  a  certainty. 
The  extreme  displacement  outward  of  the  apex  beat  would 
also,  in  the  absence  of  careful  percussion,  have  been  misleading, 
suggesting  valvular  disease. 

Much  difficulty  is  also  apt  to  arise  in  cases  such  as  the 
following,  where  there  is  little  or  no  systohc  murmur  audible 
over  the  tricuspid  valve,  but  in  which  there  is  a  well-marked 
systolic  murmur  audible  in  the  second  and  third  interspaces 
near  the  sternum.  In  such  cases  there  is  a  considerable  danger 
of  mistaking  this  murmur  for  one  arising  at  the  aortic  orifice, 
and  the  writer  has  a  very  distinct  recollection  of  a  systolic 
murmur    being    demonstrated    in    a    large    tutorial    class    at 


222  DILATATION  OF  THE  RIGHT  VENTRICLE 

Edinburgh  in  his  student  days  as  one  due  to  aortic  stenosis, 
which  did  not,  to  his  mind,  fulfil  the  requirements  of  an  aortic 
systolic  murmur,  and  which  was  certainly  this  superior  vena 
cava  murmur  of  which  we  are  speaking. 

The  following  is  a  well-marked  case  showing  this  murmur  : 

The  patient  was  a  man  aged  sixty-two,  who  was  admitted 
to  the  Birmingham  General  Hospital  some  years  ago,  under  my 
care,  suffering  from  shortness  of  breath  and  dropsy.  He  had 
well-marked  atheroma  of  his  arteries,  and  there  was  a  well- 
marked  systoHc  murmur  audible  over  the  second  right  inter- 
space close  to  the  sternum,  and  conducted  upwards  into  the 
neck.  This  murmur  might  easily  be  mistaken  for  one  of  aortic 
origin.  The  followng  characters  showed  that  it  was  not.  The 
murmur  was  more  loudly  heard  over  the  second  right  inter- 
space than  it  was  in  the  neck.  This,  as  has  been  pointed  out, 
w^as  against  it  being  of  aortic  origin. 

Again,  on  comparing  the  relative  loudness  of  the  first  sound 
and  the  murmm*  it  was  quite  clear  that  the  first  sound  of 
the  heart  was  more  perfectly  conducted  along  the  arteries 
of  the  neck  than  the  murmur  was.  This  would  not  be  the 
case  if  the  murmur  were  being  conducted  along  the  arteries. 
If  both  the  murmur  and  the  iirst  sound  were  being  conducted 
along  the  same  channel  the  loudness  of  the  two  sounds  oudit 
to  bear  a  constant  relation  to  each  other,  and  one  w-ould  not 
vary  materially  without  the  other.  This  fact  that  the  first 
sound  of  the  heart  was  conducted  along  the  carotids  more  per- 
fectly than  the  murmur,  was  conclusive  evidence  to  my  mind 
against  the  aortic  origin  of  the  murmur. 

In  spite,  therefore,  of  the  inherent  probability,  in  view  of  the 
atheroma  of  his  arteries,  that  the  murmur  was  due  to  roughen- 
ing of  the  aortic  orifice,  I  was  compelled  to  diagnose  the  murmur 
as  being  due  to  tricuspid  regurgitation,  and  this  also  in  spite  of 
the  fact  that  there  was  no  murmur  audible  over  the  tricuspid 
valve  or  over  the  right  ventricle. 

After  a  few  days'  rest  in  bed  and  tonic  treatment,  the  cedema 
subsided  and  the  murmur  became  variable — as  was  to  be  expected 
considering  its  tricuspid  origin — and  soon  entirely  disappeared 
and  thus  justified  what  appeared  to  some  of  those  who  examined 
the  patient,  a  *  foolishly  fanciful  '  diagnosis,  considering  the 
reasonable  probability  of  an  aortic  murmur  being  present.  On 
referring  to  the  notes  of  the  case,  I  found  that  mv  then  house 


DIAGNOSTIC  DIFFICULTIES  223 

physician,  relying  on  the  orthodox  description  of  the  aortic 
systohc  murmur,  preferred  to  enter  up  the  case  in  the  records 
as  one  of  '  aortic  disease.' 

Considering  the  difference,  both  as  to  prognosis  and 
treatment,  between  aortic  disease  and  tricuspid  regurgitation, 
the  importance  of  clearly  recognising  the  points  of  diagnostic 
value  is  evident,  more  especially  as  the  diagnosis  is  often 
not  easy — as  the  last  case  I  have  quoted  testifies. 

The  signs  of  diagnostic  value  to  which  I  would  draw  attention 
are  as  follows  : — 

(a)  The  character  of  the  murmur. — It  is  apt  to  be  softer 
and  more  blowing  in  tricuspid  regurgitation,  though  not 
invariably  so. 

{h)  The  nature  of  the  vessel  up  which  the  murmur  is  con- 
ducted.— It  is  not  always  as  easy  to  determine  this  as  might 
be  supposed,  because  of  the  close  proximity  of  the  veins  and 
arteries.  The  character  of  the  pulsation  is  often  a  useful 
guide,  being  weaker  and  more  fluttering  in  the  veins,  stronger 
and  more  even  in  the  arteries.  Also  the  pulsating  parts  of 
the  vessel  can  often  be  felt  to  come  to  an  end  suddenly  in 
the  case  of  a  vein,  owing  to  the  regurgitation  being  arrested 
by  a  competent  valve. 

(c)  The  relative  loudness  of  the  murmur  in  the  neck  as 
compared  with  its  loudness  in  the  second  right  interspace 
may  prove  of  service  for  diagnosis.  In  the  case  of  the  aorta, 
the  loudness  in  the  neck  is  always  equal  or  nearly  equal  to 
its  loudness  over  the  second  rib  or  interspace. 

In  the  case  of  the  murmur  of  tricuspid  origin,  its  loudness 
in  the  neck  depends  upon  the  degree  to  which  the  valves 
in  the  veins  have  given  way.  If  there  be  free  regurgitation 
up  the  veins,  the  murmur  may  be  as  well  conducted — at  all 
events  for  a  short  distance — as  the  aortic  murmur  is.  As  a 
rule,  however,  this  is  not  the  case,  and  the  conduction  is  not 
loud. 

{d)  Another  important  diagnostic  sign  is  the  relationship 
between  the  loudness  of  the  first  sound  and  the  murmur  as 
heard  in  the  arteries  of  the  neck.  If,  as  in  the  last  case  referred 
to,  the  first  sound  of  the  heart  can  be  heard  over  the  arteries 
m  the  neck,  while  the  murmur  is  heard  faintly  or  not  at  all, 


224 


DILATATION  OF  THE  RIGHT  VENTRICLE 


it  is  strong   evidence   against   the  murmur  being  of  aortic 
origin. 

The  following  case  of  a  superior  vena  cava  murmur  is  of 
sufficient  interest  to  make  it  Avortli  recording  here. 

The  patient  was  a  boy  aged  fourteen,  who  was  suffering 
from  a  rapidly  developing  attack  of  pneumonia  with  the  usual 
adolescent  type  of  upward  dilatation  of  the  right  ventricle. 

There  was  only  half  an  inch  or  so  of  relative  dullness  in  the 

Systolic  Murmur  Arising  in  the  Superior  Vena  Cava 


Area,  of 

(S^udition  of 
^mp.vencb  cavc 
xnizrinur 


{Pulmonary 
'\  sy^stolic 

systolic 
murmur 


Fig.  58. 

Thomas  W.,  aged  fourteen.  Acute  imeumonia.  Loud  pul- 
monary and  superior  vena  cava  miirniurp.  High  gastric  resonance. 
Paint  mitral  systolic,  pulmonary  second  somid  not  loud.  Veins 
of  neck  not  full.  Ai'oa  of  audition  of  murmurs  shown  by  dotted 
shadincf. 


second  left  interspace  ;  but  in  the  third  space  there  was  relative 
dullness  and  pulsation  to  the  nipple  hue  (about  2  inches  from 
the  sternum),  and  in  the  fourth  to  the  anterior  axillary  line 
3|  inches  from  the  sternum.  The  diaphragm  was  high  on 
the  left  side,  for  there  was  full  gastric  resonance  in  the  fifth 
interspace  for  nearly  3  inches  ;  but  beyond  this  point  there 
was  cardiac  pulsation  due  to  the  apex  beat,  wdiich  was  palpable 
3 1  inches  from  the  lateral  sternal  line.  On  the  right  side  the 
diaphragm — as  judged  by  the  level  of  the  liver  dullness — 
was  normal  [vide  fig.  58). 


DIAGNOSTIC  DIFFICULTIES  225 

There  was  no  increase  of  the  cardiac  dullness  to  the  right, 
and  no  excess  in  the  amount  of  right  ventricular  pulsation 
palpable  to  the  left  of  the  sternum,  and  there  was  no  tri- 
cuspid systohc  murmur ;  the  first  sound  was  clear  and  sharp 
over  the  lower  end  of  the  sternum  and  over  the  liver. 

The  pulmonary  second  sound  was  not  accentuated  and 
was,  if  anything,  less  loud  than  normal.  Also  there  was  no 
over-fullness  of  the  neck  veins. 

In  spite,  however,  of  all  these  signs  that  the  right  ventricle 
was  neither  distinctly  dilated  to  the  right  not  developing  more 
force  than  normal,  there  was  a  very  loud  murmur  which, 
from  its  point  of  maximal  loudness  and  its  direction  of  con- 
duction, must  have  been  produced  in  the  superior  vena  cava 
and  caused  by  tricuspid  regurgitation. 

It  had  its  point  of  maximal  loudness  in  the  third  and 
second  right  interspaces,  and  was  heard  well  over  a  con- 
siderable part  of  the  right  pectoral  region  to  beyond  the 
right  nipple  line,  and  loudly  conducted  into  the  veins  of  the 
neck. 

This  case  is  not  very  easy  of  explanation. 

The  presence  of  a  high  diaphragm  in  a  case  of  acute  pneu- 
monia is  suggestive  of  muscular  weakness  of  the  heart,  as  is 
also  the  fact  that  the  only  sign  of  increased  right  ventricular 
action  was  a  slight  mcrease  in  the  loudness  of  the  right  ventri- 
cular first  somid,  although  the  ventricle  must  have  been  embar- 
rassed not  only  by  the  pneumonia,  but  also  by  the  failure  of  the 
left  ventricle,  which  was  shown  by  its  dilatation  and  the  presence 
of  a  faint  mitral  systohc  murmur. 

The  outward  dilatation  in  the  third  left  interspace  and  a 
well-marked  pulmonary  systolic  murmur  also  pointed  to  over- 
strain of  the  right  side  of  the  heart. 

The  reason  for  the  absence  of  more  signs  of  venous  engore- 
ment  must  be  sought  for  in  the  supposition  that  the  muscular 
tone  of  the  vems  was  good,  and  the  reason  for  the  loudness 
of  the  superior  vena  cava  murmur  in  the  supposition  that 
for  some  reason  or  other  (possibly  dependent  on  the  great 
dilatation  to  the  left  and  on  the  presence  of  the  pneumonia), 
the  superior  vena  cava  was  more  constricted  than  it  usually 
is  at  the  point  where  it  passes  through  the  pericardium. 


226         DILATATION  OF  THE  EIGHT  VENTRICLE 

Arterial  Compression  Murmur 

In  connection  with  the  diagnosis  of  systohc  murmurs, 
audible  along  the  line  of  the  vessels,  it  is  well  to  remember 
the  possibility  of  a  systolic  murmur  being  produced  in  the 
subclavian  artery  itself.  T-his  murmur,  which  is  audible  in  the 
region  of  the  clavicles,  may,  without  proper  care,  be  mistaken 
for  a  systolic  pulmonary  one  or  else,  if  well  marked  on  the  right 
side,  for  a  murmur  due  to  tricuspid  regurgitation.  In  character 
it  is  a  sharp  blowing  systolic  murmur  audible  more  or  less 
widely,  whose  point  of  maximal  loudness  lies  at  about  the 
spot  where  the  subclavian  artery  crosses  the  first  rib.  The 
murmur  often  closely  resembles  a  loud  pulmonary  or  aortic 
systolic  murmur  or  a  loud  superior  vena  cava  murmur,  but  it 
can  be  at  once  distinguished  by  two  characteristics :  firstly, 
the  situation  of  its  point  of  maximal  intensity ;  and  secondly, 
the  fact  that  it  can  be  caused  to  disappear  by  altering  the 
position  of  the  shoulder. 

There  seems  no  doubt  that  it  is  produced  in  the  subclavian 
artery,  at  the  point  where  it  crosses  the  first  rib,  and  it  probably 
is  caused  by  compression  of  a  badly  filled  artery  at  this  point. 

Without  due  care  this  murmur  is  quite  apt  to  cause  an 
error  in  diagnosis. 

It  is  specially  common  in  young  women  with  anabmia. 

A  similar  murmur  can  often  be  easily  produced  by  too 
firm  pressure  of  the  stethoscope  over  the  subclavian  artery 
below  the  clavicle. 


PART  II.-ESSAYS  DEALING  MAINLY  WITH 
DILATATION  OF  THE  HEART  DUE  TO 
OVERSTRAIN 


Essay  V.— THE  CONDITION  OF  THE  HEART  IN 
THE  ANEMIA  OF  ADOLESCENCE 

The  cases  of  anaemia  studied  in  this  research  were  almost 
entirely  the  ordinary  cases  of  chlorosis  and  anaemia  which 
occm-  so  fi-equently  when  yomig  women  of  eighteen  to  twenty- 
two  engage  in  manual  work  under  the  unsatisfactory  conditions 
which  used  often  to  be  associated  with  work  in  factories  and 
workshops.  I  have  excluded  cases  where  the  anaemia  was 
definitely  secondary  to  such  diseases  as  phthisis  and  chronic 
nephritis,  because  the  cardiac  phenomena  are  usually  different 
from  those  which  occur  in  the  simple  anaemia  of  adolescence. 
In  the  cases  dealt  with  in  this  essay,  the  anaemia  was  a 
purely  functional  one,  and  subsided  on  the  adoption  of 
treatment  by  rest  and  iron. 

As  Regards  the  Method  of  Examination 

The  patients  were  as  a  rule  examined  in  the  recumbent 
attitude  and  often  when  erect  as  well.  In  connection  with  the 
somewhat  extreme  amount  of  dilatation  which  is  often  noted, 
the  following  facts  must  be  remembered  : — 

1.  This  research  deals  with  a  consecutive  series  of  cases 
observed  twenty  years  ago  when  the  conditions  of  factory 
labour  were  more  calculated  to  produce  anaemia  than  they 
are  at  the  present  day. 

2.  The  heart  was  often  percussed  with  the  lungs  as  fully 
deflated  as  the  patient  was  able  to  manage — so  as  to  get  as 
nearly  as  possible  the  absolute  size  of  the  heart. 

227  q2 


228  HEART  FAILURE 

3.  As  the  patients  were  not  examined  oftener  than  once 
a  week,  and  always  improved  under  treatment,  it  follows 
that  the  greatest  amomit  of  cardiac  dilatation  was  found  on  first 
examming  the  patient.  Now  the  subjects  of  this  type  of 
anaemia  are  mainly  young  women  from  seventeen  to  twenty-one 
years  of  age,  in  w^hom  a  careful  examination  of  the  chest  at 
their  first  visit  to  a  hospital  is  apt  to  be  accompanied  by  a 
certain  amount  of  nervousness.  This  nervous  excitement 
would  natm-ally  tend  to  exaggerate,  temporarily,  such  cardiac 
dilatation  as  was  already  present.  Even  though  such 
temporary  exaggeration  of  the  amount  of  dilatation  were 
present,  however,  it  does  not  in  the  least  detract  from  the 
value  of  the  symptoms  presented  or  the  evidence  they  afford 
as  to  the  changes  which  take  place  when  the  heart  fails,  in 
consequence  of  anaemic  malnutrition.  From  this  research,  I 
have  excluded  all  cases  where  the  failure  of  the  right  ventricle 
was  secondary  to  organic  valvular  disease  of  the  heart. 

The  Condition  of  the  Heart  in  the  Anemia  of 
Adolescence 

The  careful  clinical  study  of  the  heart  in  anaemia,  which 
this  research  entailed,  demonstrated  quite  clearly  that  the 
most  important  change,  which  occurs  Avhere  heart  failure 
accompanies  the  anaemia  of  adolescence,  is  a  dilatation  of 
the  right  ventricle. 

Evidences  of  Dilatation  of  the  Eight  Ventricle 

Inspection  and  palpation  m  cases  of  anaemic  dyspnoea 
in  adolescents  give  the  physical  signs  of  enlargement  of  the 
heart,  which  have  been  already  described  (pp.  14,  25)  as 
characterising  dilatation  of  the  conus  arteriosus  of  the  right 
ventricle. 

Dilatation  Up\vards  and  to  the  Left 

Percussion  of  the  heart  in  cases  of  anaemic  heart  failure 
reveals  the  fact  that  there  is  an  enlargement  of  the  heart  in 
the  third  and  second  left  interspaces  in  the  great  majority 
of  those  who  are  suffering  from  dyspnoea  due  to  this  cause. 


IN  THE  ANEMIA  OF  ADOLESCENCE  229 

The  following  statistics  bearing  upon  this  point  were 
gathered  in  my  out-patient  department  at  the  Birmingham 
General  Hospital  in  the  twenty-one  months  between  September 
1890  and  May  1892.  During  this  period,  350  cases  of  this  type 
of  anaemia  were  seen.  In  63  cases  no  notes  were  taken,  and 
only  the  remaining  287  are  therefore  available  for  study. 

Out  of  the  287  cases  of  anaemia,  the  heart  was  normal  in 
45,  and  showed  some  signs  of  failure  in  242. 

The  presence  or  absence  of  dilatation  of  the  heart  upwards 
and  to  the  left  in  the  second  and  third  left  interspaces  was 
noted  in  220  cases  out  of  the  242,  and  the  results  will  best 
be  stated  in  tabular  form. 

Cases  of  Simple  Anaemia  seen  between  September  1890 
AND  May  1892 

No  detailed  notes  taken        .... 

Heart  normal      ...... 

Some  cardiac  failure,  but  character  not  noted  . 

Dyspnoea,  but  no  dilatation  in  second  inter- 
space     ....... 

Upward  dilatation  of  the  right  ventricle 
'  present,'  only  '  very  slight,'  or  '  amount 
not  noted  "...... 

Amount  of  dilatation  carefully  noted 


With  regard  to  the  167  carefully  noted  cases — 

In  73  of  them  the  amount  of  relative  cardiac  dullness 
in  the  second  left  interspace  was  1  inch  or  less  in 
extent  (in  35  it  was  1  inch  in  extent). 

In  71  patients  the  relative  dullness  in  the  second  left  inter- 
space was  more  than  1  inch  in  width.  Out  of  these 
71  cases  there  was  more  than  1|  inches  of  dullness  in 
27  patients. 

In  23  patients,  although  there  was  no  cardiac  dullness 
in  the  second  interspace,  there  was  a  distinct  increase 
of  the  dullness  in  the  third  left  interspace. 


63 

cases 

45 

j> 

22 

5> 

35 

55 

18 

55 

167 

55 

350 

55 

230 


HEART  FAILURE 


The  exact  amounts  of  relative  dullness  in  the  second  left 
interspace  in  the  167  patients  were  as  follows  : — 


In  19  patients  there  was  |  inch  of  relative  dullness. 


73 


In  17  patients  there  was  1|  inches  of  relative  dulhiess. 


„27 

}f 

>) 

n 

5J 

5)                    55                         5 

„    7 

J  J 

>5 

If 

JJ 

55                      55                           5 

„u 

J5 

); 

2 

J> 

55                       55                           5 

„    B 

more 

than  2 

JJ 

55                       55                           5 

„    3 

there 

was 

3 

„  or 

more  ,,           , 

71 


In  23  patients  there  was  no  relative  dullness  in  the  second 
left  interspace,  but  there  was  increase  of  relative  dullness  in  the 
third  interspace — 1|-  inches  being  taken  as  the  normal  amount. 

In  14  patients  there  was  2  inches  of  relative  dullness. 
K  91 

55  "  5)  55  55  •"2        "  "  "  " 

9  R 

5  5  ■"  5  5  5  1  5  5  "  5  5  5  5  5  5  5  5 

,,     2       ,,  ,,         ,,  '  some  dilatation  ' 


In  many  cases,  whore  there  was  more  than  one  inch 
of  relative  dullness  in  the  second  left  interspace  there  was 
pulsation  to  be  seen  and  felt.  In  some  there  was  absolute 
dullness  as  well  as  relative  {vide  fig.  77,  p.  268). 

It  must  therefore  be  acknowledged  that  increase  of  the 
cardiac  dullness  upwards  and  to  the  left  is  very  frequent  in 
cases  of  anaGmia  with  heart  failure,  for  it  occurred  in  185  out 
of  350  cases — that  is,  in  54  per  cent. 

If,  however,  the  cases  showing  signs  of  heart  failure  alone 
are  considered,  the  frequency  of  this  type  of  dilatation  is  found 
to  be  at  least  84  per  cent. 


IN  THE  ANiEMIA  OF  ADOLESCENCE  231 

It  can  therefore  be  definitely  asserted  that  increase  of  the 
heart  upwards  and  to  the  left  in  the  second  and  third  left 
interspaces  is  usually  found,  whenever  marked  dyspnoea 
accompanies  the  simple  anaemia  of  adolescence. 

The  Cause  of  the  Upwakd  Increase  of  the  Heart 

The  question  must  now  be  answered :  To  what  is  this 
increase  in  the  cardiac  duUness  in  the  second  left  interspace 
due  ?  It  might  be  due  to  the  left  auricle,  the  pulmonary 
artery,  or  to  an  upward  increase  of  the  right  ventricle. 

This  Increase  in  the  Cardiac  Dullness  is  not  Due 
TO  THE  Left  Auricle 

In  all  cases,  where  the  cardiac  dullness  in  the  second  left 
interspace  is  well  marked,  there  is,  as  a  rule,  visible  pulsation 
as  weU  ;  therefore  it  is  quite  eas}^  to  determine  the  nature 
of  this  pulsation,  if  the  cardiac  sounds  be  followed  by  the 
stethoscope  at  the  same  time  that  its  rhj-thm  be  watched. 
When  this  is  done,  the  pulsation  is  fomid  to  be  certainly  systolic 
and  not  pre-systolic  in  rhythm.  I  have  studied  this  rhythm 
in  many  hundreds  of  cases,  and  in  no  more  than  one  or  two, 
at  most,  have  I  failed  to  satisfy  myself  of  its  systolic  nature. 
On  first  commencing  this  research,  I  was  under  the  impression 
that  the  pulsation  was  due  to  the  amicle,  as  brief  notes  made 
of  my  out-patients  at  the  hospital  in  1889  and  1890  testify; 
and,  therefore,  the  conviction  that  it  is  always  systohc  (at 
which  I  very  speedily  arrived)  is  the  result  of  observation 
and  not  of  theory.  Cardiographic  observations — of  which  I 
have  taken  some  himdreds — have  also  demonstrated  this 
same  fact. 

It  is,  however,  physically  possible  for  a  distended  left 
auricular  appendix  to  reach  the  chest  wall  in  the  second  left 
interspace,  as  may  be  demonstrated  if  the  left  side  of  the  heart  be 
distended  iji  situ  by  hard  parafiin,  when  the  right  side  is  empt5^ 
There  is,  however,  good  reason  to  doubt  if  this  ever  actually 
occurs  cUnically,  for  the  distended  right  side  of  the  heart  will 
prevent  the  appendix  from  reaching  the  anterior  chest  wall. 


232  ANiEMIA  OF  ADOLESCENCE 

Increase  of  Cardiac  Dullness  not  Due  to  the 
Pulmonary  Artery. 

That  it  is  not  due  to  the  pulmonary  artery  is  shown  by  the 
use  of  the  cardiograph,  for  the  auricular  wave  is  shown  in  a 
manner  that  would  be  impossible  in  the  case  of  the  pulmonary 
artery.  Also  by  carefully  timing  the  pulsation,  the  maximum 
rise  can,  not  infrequently,  be  clearly  seen  to  be  systolic  in 
rhythm,  and  to  subside  considerably,  before  the  second  sound 
of  the  heart,  in  a  way  that  could  not  occur  if  it  were  due  to 
the  pulmonary  artery. 

Further,  in  well-marked  cases,  the  shock  due  to  closure 
of  the  semilunar  valves  can,  sometimes,  be  clearly  felt  at  the 
upper  level  of  the  dull  area  (p.  286).  In  no  case  have  I  been 
able  to  find  any  evidence  that  it  was  due  to  the  pulmonary 
artery.  That  it  is  due  to  one  of  the  ventricles  is  shown  by  the 
above  observations. 

Increase  of  Cardiac  Dullness  Due  to  Eight 
Ventricle 

That  it  is  due  to  the  right  ventricle  is  shown,  firstly,  by 
the  fact  that  the  amount  of  the  pulsation,  observable  over  the 
dull  area,  varies  with  respiration.  It  is  most  marked  at  the 
end  of  expiration.  That  this  is  not  due  to  the  recession  of 
the  lungs,  during  expiration,  is  shown  by  the  fact  that  it  is 
not  so  well  marked  when  the  chest  is  held  in  the  position  of 
full  expiration,  as  it  is  during  ordinary  breathing. 

It  cannot  be  beUeved  that  the  left  ventricle  could  be 
influenced  to  this  extent  by  the  respiratory  movements.  But, 
considering  the  relatively  low  pressure  in  the  right  ventricle, 
it  is,  I  think,  to  be  expected  that  the  variation  in  the  intra- 
thoracic pressure,  which  results  from  the  respiratory  move- 
ments, would  influence  the  filling  of  the  heart  sufficiently  to 
cause  the  above-mentioned  variation.^ 

1  Numerous  observations  made  by  the  writer  in  recent  years  on  the  heart 
Bounds  prove  that  the  sounds  duo  to  the  right  ventricle  are  very  frequently 
louder  at  the  end  of  inspiration  than  at  any  other  time  in  the  respiratory 
cycle,  the  same  variation  not  being  observable  in  the  case  of  the  left  ventricle. 


UPWARD  DILATATION  OF  RIGHT  VENTRICLE    233 

Pathological  Proof. — I  have  seen  many  post-mortems 
on  well-marked  cases  of  anaemia,  and  have  frequently  distended 
the  heart  with  hard  paraffin  in  situ  in  such  cases,  and  the 
pathological  evidence  is  clear  that  the  upward  enlargement 
of  the  heart  is  due  to  dilatation  of  the  right  ventricle. 

The  following  are  the  notes  with  regard  to  the  relation  of 
the  undistended  heart  to  the  chest  wall  in  one  such  case,  and 
of  the  distended  heart  in  another  case  : — 

Kate  G.,  aged  fifteen.  Extremely  ansemic.  Heart  extremely 
dilated,  with  well-marked  pulmonary  murmur. 

The  relative  dullness  of  the  heart  durmg  life  was  as 
follows  : — 

About  1^  inches  in  second  left  interspace. 
,,       ig       "       >'  tnn'd       ,,  ,, 

,,        ^  inch       ,,  third  right  ,, 

„      1       „         „  fourth  „ 

Apex  fifth  left  space  in  the  nipple  line. 

The  girl  died,  suddenly,  three  days  after  the  above  notes 
were  made. 

The  following  notes  were  made  as  to  the  position  of  the 
heart  in  relation  to  the  chest  wall  at  the  post-mortem 
examination  : — 

Right  ventricle. — The  conus  arteriosus  is  much  dilated 
upwards,  and  reaches  from  the  right  edge  of  the  sternum  in  the 
first  space  to  the  lower  border  of  the  first  rib  on  the  left,  and 
extends  for  1|  inches  in  the  second  left  space. 

The  pulmonary  valves  were  under  the  lower  border  of  the 
first  rib  ;  the  pulmonary  artery  in  its  collapsed  condition  looked 
crumpled  and  irregular,  and  the  dilated  upper  border  of  the 
conus  arteriosus  overhung  it. 

In  another  case,  an  equal  degree  of  dilatation  of  the  upper 
part  of  the  right  ventricle  was  observable.  The  following  are 
the  details  of  this  case  : — 

The  patient  was  a  j^oung  man  suffering  from  a  rapidly 
progressing  pernicious  anaemia. 

In  this  case  also,  the  conus  arteriosus  of  the  right  ventricle 
extended  from  the  second  right  costal  cartilage  upwards  to  the 


234  ANiEMIA  OF  ADOLESCENCE 

lower  part  of  the  first  rib,  and  outwards  in  the  second  left  space 
as  far  as  the  nipple  line. 

It  is  needless  to  say  that  here,  as  in  the  last  case,  the  left 
auricular  appendix  in  its  relaxed  condition  was  completely 
hidden  behind  the  dilated  right  ventricle.     The  right  auricular 
appendix  came  up  as  high  as  the  first  right  space,  and  its  tip* 
reached  to  the  middle  line  of  the  sternum. 

The  apex  was  in  the  fourth  space,  one  inch  external  to  the 
nipple  line. 

This  is,  in  fact,  the  type  of  dilatation  already  fully  described 
at  pp.  12  and  25,  and  also  dealt  with  at  p.  330,  and  is  the  usual 
type  that  occurs  in  the  right  ventricular  failure  in  valvular 
disease  in  puberty  and  adolescence. 

In  such  cases,  this  type  of  dilatation  is  often  extreme 
m  amount,  and  it  is  not  very  uncommon  to  find — if  the  heart 
be  distended  w  situ  with  hard  paraffin — at  the  post-mortem, 
that  there  is  so  much  upward  dilatation  of  the  conus  arteriosus 
of  the  right  ventricle  that  the  pulmonary  valves  he  in  the 
upper  part  of  the  second  left  interspace  or  even  mider  the 
first  rib. 

For  further  proof,  see  also  p.  247. 

Consequences  of  this  Type  of  Dilatation  of  the  Piight 
Ventkicle. — The  most  important  change  resulting  from  this 
dilatation  is  an  alteration  m  the  relationships  of  the  pulmonary 
artery,  whereby  a  murmur  is  apt  to  be  produced  Avith  each 
systole  of  the  ventricle.  The  further  discussion  of  this  point 
will  be  taken  up  later  on,  when  the  cardiac  murmurs  which 
occur  in  anaemia  are  considered. 

Displacement  of  the  Apex  Upwards. — Another  striking 
change,  which  is  noticeable  in  cases  of  heart  failure  in  anaemia, 
is  the  upward  displacement  of  the  apex.  This  change  is 
described  by  the  late  Dr.  Foxwell,^  and  the  conclusions  at 
which  I  have  arrived,  as  the  result  of  my  observations,  are, 
in  the  main,  identical  with  his.  This  upward  displacement  of 
the  apex  is  common  in  this  type  of  heart  failure.  Thus  out 
of  a  total  of  192  cases,  where  there  was  upward  dilatation  of 
the  right  ventricle,  the  apex  was  above  the  level  of  the  fifth 
interspace  in  87 — i.e.,  in  45' 3  per  cent. 

^  Essays  in  Heart  and  Lung  Disease,  vide  p.  238. 


DISPLACEMENT  OF  APEX  UPWARDS  235 

In  one- quarter  of  these  87  cases  the  elevation  was  not 
very  great,  and  the  apex  was  described  as  being  under  the  fifth 
rib.  In  some  of  these  last-named  cases  the  apex  was  palpable 
in  the  fourth  interspace  when  the  patient  was  recumbent,  but 
could  be  felt  in  the  upper  part  of  the  fifth  interspace,  when 
the  patient  was  erect. 

It  is  safe  to  say  that  in  nearly  half  the  cases  of  well-marked 
upward  dilatation  of  the  right  ventricle  in  anaemia,  there  is 
upward  displacement  of  the  apex. 

The  following  are  some  cases  which  illustrate  this  upward 
displacement  of  the  apex. 

Firstly,  an  extreme  case  is  the  following  : — 

A  young  woman  suffering  from  anaemia  and  dyspncea  had 
so  great  an  amount  of  dilatation  of  the  conus  arteriosus  and 
adjacent  part  of  the  ventricle,  combined  with  upward  displace- 
ment of  the  apex,  that  there  was  well-marked  cardiac  pulsation 
for  more  than  2  inches  in  the  second  left  interspace,  while 
the  main  cardiac  impulse  was  in  the  third  interspace,  and 
there  was  no  cardiac  pulsation  in  the  fourth  interspace,  except 
during  inspiration,  when  the  elevation  of  the  ribs  allowed  of 
the  apex  being  felt  in  the  upper  part  of  that  interspace. 
Cardiograms  taken  in  the  third  interspace  showed  the  pulsation 
there  to  be  of  the  true  apex  type  {vide  p.  298). 

The  following  case,  although  not  one  of  anaemia,  is  of 
exceptional  interest,  because  it  throws  some  light  upon  the 
cause  of  the  changes  in  the  heart,  which  we  are  now  discussing. 
For  permission  to  refer  to  it,  I  am  indebted  to  my  colleague 
Sir  Kobert  Simon,  under  whose  care  the  patient  was,  while  an 
in-patient  in  the  Birmingham  General  Hos.pital. 

Case  showing  displacement  of  apex.  The  girl,  aged  about 
fifteen,  had  suffered  from  occasional  fainting  attacks  for  some 
years  before  I  first  saw  her  in  October  1891,  and  after  each  faint- 
ing attack,  she  suffered  from  dyspnoea,  which  had  increased 
latterly.  During  the  last  few  months,  cyanosis  had  developed. 
When  I  saw  her,  the  heart  presented  a  condition  similar  to 
that  above  described.  There  was,  however,  no  haemic  murmur 
in  the  second  space,  and  there  was  cyanosis  instead  of  anaemia. 

She  shortly  after  developed  thrombosis  of  the  right  sub- 
clavian vein,  and  was  admitted  to  the  hospital,  where  she 
remained    till    death,    four    months    later.     The    thrombosis 


236  ANEMIA  OF  ADOLESCENCE 

subsided,  but  her  cardiac  condition  remained  unaltered,  and  she 
died  of  heart  failure.  The  post-mortem  showed  no  organic 
disease  of  any  sort.  The  right  side  of  the  heart  was  dilated, 
the  left  side  rather  smaller  than  normal,  and  the  aorta  was  very 
much  narrowed.  The  narrowing  was  at  first  thought  to  be 
congenital,  but  I  now  believe  it  to  be  simply  due  to  the  lessened 
work  thrown  on  the  left  ventricle. 

Some  idea  of  the  dilatation  of  the  right  ventricle  will  be 
given  by  the  following  iigures  : — 

The  total  circumference  of  the  heart  was  11 1  inches.  Of  this, 
7  inches  belonged  to  the  right  and  4J  inches  to  the  left  ventricle. 
The  left  ventricle  was  situated  wholly  posteriorly,  and  the  right 
ventricle  occupied  the  whole  of  the  front  and  sides  of  the  heart. 

As  to  the  cubic  contents  of  the  chambers  (measured  by 
distensible  india-rubber  bags  under  a  pressure  of  about  2  feet 
of  water)  it  was  as  follows  : — 

Left  ventricle,  90  c.c.  (i.e.  about  normal). 

Left  auricle,  35  c.c.  (normal,  90  c.c.  more  or  less). 

Eight  ventricle,  160  c.c. 

Eight  auricle,  215  c.c. 

The  right  auricle  only  projected  1|  inches  to  right  of  the 
middle  line.  The  tip  of  its  appendix  was  under  the  sternal 
end  of  the  second  left  rib.  The  auriculo-ventricular  groove 
was  wholly  to  the  left  of  the  sternum,  and  it  commenced  above 
at  the  lateral  sternal  line,  under  the  second  rib,  and  ran  down- 
wards and  slightly  outwards  to  the  level  of  the  fifth  costal  carti- 
lage at  I  inch  to  the  left  of  the  lateral  sternal  line.  This  point 
was  as  low^  as,  if  not  lower  than,  the  level  of  the  apex,  which 
was  situated  in  the  upper  part  of  the  fifth  space  in  the  anterior 
axillary  line. 

The  natm-e  of  this  case  is  extremely  obscm'e,  and  I  can  only 
explain  it  by  supposing  some  hindrance  to  the  passage  of  the 
blood  through  the  lungs.  Nothing  definite  was,  however, 
found  that  would  clear  up  this  point. 

The  interesting  point  about  this  case  is,  that  we  have  here 
a  case  of  dilated  and  hypertrophied  right  ventricle  uncom- 
phcated  by  other  disease,  and  it  presents  just  the  clinical 
appearances  of  the  dilated  heart  of  anaemia,  and  helps  to 
elucidate  the  question  we  are  now  discussing  as  to  the 
displacement  of  the  apex  beat. 


DISPLACEMENT  OF  APEX  UPWARDS  237 

In  the  present  instance,  the  axis  of  the  heart  seemed  much 
more  horizontal  than  usual,  and  the  position  and  direction 
of  the  auriculo-ventricular  groove  was  altered.  It  was  wholly 
displaced  to  the  left  (probably  by  the  distension  of  the  right 
auricle),  and  its  lower  end  was  also  swung  to  the  left. 

This  rotation  would,  of  course,  tend  to  raise  the  apex 
somewhat,  and  its  influence  w^ould  be  added  to  the  other 
agencies  at  work. 

As  regards  the  cause  of  this  displacement  of  the  apex : — 

1.  Some  part  of  the  displacement  may  be  only  apparent, 
due  to  the  distension  of  the  right  ventricle  preventing  the 
true  apex  from  striking  or  even  coming  near  to  the  chest 
wall. 

2.  A  part  of  the  displacement  may  sometimes  be  due  (as 
seemed  to  be  the  case  in  the  patient  referred  to  on  p.  353)  to 
the  distension  of  the  ventricle  downwards.  I  think  this  is 
improbable  in  most  cases  of  anaemia,  because  we  rarely 
find  any  dilatation  of  the  right  auricle. 

3.  A  rise  in  the  average  level  of  the  diaphragm  does, 
undoubtedly,  play  some  part  in  causing  a  rise  in  the  heart's 
apex  in  some  cases  of  anaemia,  but  in  the  statistics  here  quoted 
this  point  had  not  been  recognised  and  was  therefore  not 
inquired  into. 

It  is  certain  that  a  high  apex  beat  is  often  seen  in  anaemia 
without  any  corresponding  rise  in  the  diaphragm.  The  whole 
question  of  the  exact  relationship  which  a  rise  in  the  average 
level  of  the  diaphragm  bears  to  anaemia  is  not  one  upon  which 
I  can,  at  present,  speak  definitely. 

4.  It  seems  clear  that  the  rise  of  the  apex  is  due  to  a  dilatation 
of  the  main  portion  of  the  anterior  wall  of  the  right  ventricle. 
This  increase  does  not  take  place  to  the  right — as  might  be 
expected ;  nor  forwards,  owing  to  the  support  given  by  the 
anterior  chest  wall;  nor  backwards,  because  of  the  strength 
of  the  interventricular  septum,  and  therefore  has  to  take 
place  to  the  left.  To  do  so,  the  left  ventricle  has  to  move 
outwards,  and  can  only  do  so  by  swinging  round  its  fixed  point 
at  the  base.  In  so  doing,  the  apex  must  move  in  the  arc  of 
a  circle,  whose  centre  is  at  the  root  of  the  aorta ;  and  the  apex 
must  therefore  move  upwards,  as  well  as  outwards,  in  order 


238  ANEMIA  OF  ADOLESCENCE 

to  give  room  for  the  expanding  right  ventricle,  as  was  pointed 
out  by  the  lato  Dr.  Foxwell  in  his  '  Essays  in  Heart  and  Lung 
Disease.' 

Eeference  to  the  figures,  showing  the  shape  of  the  heart 
in  anasmic  dyspnea  (which  are  given  on  pp.  261,  268,  289,  &c.), 
ilhistrate  this  point  as  to  the  upward  displacement  of  the  apex. 
The  discussion  of  the  various  factors  at  work  in  producing  this 
displacement  is  fully  dealt  with  in  the  essay  on  displacement 
of  the  heart. 

Geneeal  Dilatation  to  the  Eight  in  Anemia 

Another  point  of  interest  in  connection  with  this  type  of 
cardiac  dilatation  is  the  absence  of  any  enlargement  of  the 
heart  towards  the  right. 

Taking  the  relative  cardiac  dullness  to  extend  normally  for 
half  an  inch  to  the  right  of  the  sternum  (if  the  chest  is  percussed 
in  the  position  of  full  expiration),  and  reckoning  as  abnormal 
any  amount  of  relative  dullness  which  exceeds  this  half-inch, 
we  find  that  among  the  178  cases  of  well-marked  anaemic 
dilatation  of  the  heart  only  15,  or  not  quite  8-5  per  cent,  showed 
dilatation  of  the  heart  to  the  right — i.e.,  the  right  border  of 
the  heart  was  normal  in  91' 5  per  cent,  of  the  cases. 

The  relative  cardiac  dullness  in  anaemia  frequently  does  not 
reach  as  far  as  this  (which  is  given  as  the  normal  limit  of  the 
relative  cardiac  dullness  to  the  right) ;  but  the  same  can  be 
said  as  regards  the  percussion  of  any  normal  chest. 

The  further  details  as  to  the  situation  of  the  right  border 
of  the  cardiac  dullness  in  these  cases  of  anaemia  are  as  follows  : 
right  border,  |  inch  from  sternum,  23  cases  ;  J  inch,  9  cases ; 
at  right  edge  of  sternum  or  mid-sternum,  42  cases,  and  no 
definite  note  in  89  instances.  Among  the  15  cases  showing 
dilatation  to  the  right  of  the  sternum,  there  were  only  6  where 
there  was  1  inch  or  more  of  relative  dullness  on  percussion. 

In  the  face  of  such  figures  as  these,  it  can  be  asserted  that 
there  is,  as  a  rule,  no  dilatation  of  the  heart  to  the  right  in  cases 
of  simple  anaemia  in  adolescence  showing  upward  dilatation 
of  the  right  ventricle. 

This  fact  is  strons;  evidence  in  favour  of  the  statements 


NO  DILATATION  TO  THE  RIGHT  239 

advanced  in  an  earlier  essay  as  to  the  reason  why  this  type 
of  dilatation  occurs  in  adolescence. 

It  is  more  than  likely  that  this  absence  of  dilatation  to 
the  right  is  not  a  mere  coincidence,  but  that  the  two  facts 
stand  in  the  relationship  of  cause  and  effect. 

The  upward  dilatation  of  the  right  ventricle  is  caused  by 
the  intraventricular  pressure  being  in  excess  of  the  resisting 
power  of  this  the  weakest  portion  of  its  muscular  wall,  and  the 
greater  the  intraventricular  pressure  the  greater  will  be  the 
dilatation.  For  the  development  of  this  pressure  it  is  essential 
that  the  tricuspid  valve  should  bo  competent,  otherwise  the 
'  safety  valve  '  action  of  the  heart  would  come  into  play  and 
tricuspid  leakage  prevent  the  intraventricular  pressure  from 
rising  to  an  adequate  extent.  In  the  adolescent  the  softness 
of  the  fibrous  tissues,  owing  to  their  immaturity,  will  probably 
render  the  right  auricle  and  veins  less  able  to  give  support 
to  a  leaking  tricuspid  valve  than  is  the  case  Avith  the  stronger 
fibrous  tissues  of  the  adult.  Certain  it  is  that  dilatation 
of  the  right  ventricle  to  the  right  and  the  tricuspid  incom- 
petence to  which  it  leads  are  very  rarely  found  to  be  present 
in  the  heart  failure  with  upw"ard  dilatation  of  the  right  ventricle 
which  occurs  in  the  ansemia  of  adolescence. 

Frequency  of  a  Tricuspid  Systolic  Murmur 

Evidence  as  to  the  infrequence  of  general  dilatation  is 
also  given  by  noting  the  occurrence  of  a  tricuspid  systolic 
murmur  in  cases  of  heart  failure  in  anaemia.  Out  of  the  178 
cases,  the  presence  of  a  murmur  was  only  noted  in  41 
instances,  or  23  per  cent,  of  the  cases,  and  of  these  the  murmur 
was  a  faint  one  in  12  instances ;  so  it  was  well-marked  in  only 
29  patients — i.e.  in  16  per  cent.  If  the  178  cases  of  anaemia 
be  divided  into  two  groups  according  to  age,  it  will  be  found 
that  in  the  older  group  the  number  of  cases  of  tricuspid  re- 
gurgitation predominate,  thus  confirming  the  statement  made 
(p.  33)  that  the  older  the  patient  the  greater  the  tendency 
to  general  dilatation  of  the  right  ventricle  rather  than  to  the 
localised  dilatation  of  the  conus  arteriosus  and  the  adjacent 
part  of  the  anterior  wall  which  occurs  in  adolescence.     The 


240  ANEMIA  OF  ADOLESCENCE 

figures  are  as  follows  :  In  cases  of  eighteen  years  of  age  or  less, 
a  tricuspid  murmur  was  present  in  15  per  cent.,  whereas  in 
patients  of  nineteen  years  or  more  it  was  present  in  28  per 
cent,  of  the  cases. 

Out  of  the  41  patients  just  referred  to  who  had  a  tricuspid 
systolic  murmur,  only  8  gave  any  evidence  of  dilatation  of 
the  heart  towards  the  right,  and  in  the  remaining  33  the  right 
border  of  the  heart  was  normal.  This  leaves  8  cases  in  whom 
there  was  some  dilatation  to  the  right  without  any  evidence 
of  a  tricuspid  murmur.  For  illustrations  of  the  area  over 
which  the  murmurs  were  audible  in  the  above  cases  of 
anaemia,  see  figs.  75,  78,  81,  and  86-90. 

The  total  number  of  the  178  patients  who  showed  some  signs 
of  general  dilatation  of  the  right  ventricle  was  therefore  47, 
or  nearly  27  per  cent. 

Presence  of  Signs  of  Failure  of  the  Left  Ventricle 
IN  THE  Anaemia  of  Adolescence 

In  cases  of  anaemic  heart  failure,  all  evidence  seems  to 
show  that  failure  of  the  left  ventricle  is  not  ordinarily  present, 
although  it  may  sometimes  occur.  Considering  the  weakness 
of  the  right  side  and  the  amount  of  hard  work  that  some  of 
these  anaemic  girls  do  in  factories  and  elsewhere,  it  is 
interesting  that  left  ventricular  failure  is  not  more  often  seen. 
The  reason  for  this  is  to  be  found  in  the  weakness  of  the  right 
ventricle.  Failure  of  the  right  side  of  the  heart  and  the  breath- 
lessness  which  it  causes,  prevents  the  patient  from  exerting 
herself  sufficiently  to  overstrain  the  left  heart. 

The  full  statistics  of  left  ventricular  failure  are  not 
easy  to  obtain,  owing  to  the  frequency  with  which,  in  these  cases, 
the  apex  is  swung  upwards  and  outwards  to  a  point  in  the 
fourth  interspace  external  to  the  nipple  line. 

It  is  evident  that  in  such  cases  the  outward  displacement 
of  the  apex  is  no  criterion  as  to  the  presence  of  dilatation  of 
the  left  ventricle.  It  is  more  than  probable  that  this  upward 
and  outward  displacement  of  the  apex  is  evidence  that  the 
left  ventricle  is  at  most  of  normal  size  and  quite  possibly  that 
it  is  smaller  than  normal. 


NO  FAILURE  OF  LEFT  VENTRICLE  241 

This  question  is  further  discussed  at  p.  348. 

If  those  cases  only  are  considered,  where  the  apex  is  in  the 
fifth  interspace  (and  they  numher  only  93  out  of  the  178),  it 
is  found  that  22,  or  23-6  per  cent.,  had  some  outward  displace- 
ment of  the  apex,  suggesting  left  ventricular  dilatation.  Of 
these,  only  9  had  a  systohc  mitral  murmur,  and  13  had  not. 

If  the  presence  of  a  mitral  systohc  murmur  be  inquired 
into,  it  is  found  that  38  patients  out  of  the  178  had  this  murmur 
present,  or  21  per  cent. 

Taking  these  sets  of  figures  together,  it  shows  that  52 
patients  out  of  the  178,  or  29-2  per  cent.,  showed  some  signs  of 
left  ventricular  failure. 

In  connection  with  what  has  been  said  as  to  the  weakness 
of  the  thinner  part  of  the  right  ventricle  in  adolescence, 
it  is  interesting  to  find  that  on  noting  the  ages  of  the  cases 
showing  signs  of  left  ventricular  failure,  it  is  found  that  they 
mainly  occur  amongst  the  older  adolescents.  The  figures  are 
as  follows  : — 

On  dividing  the  patients  into  two  age-groups,  one  of  eighteen 
and  mider  and  the  other  of  nmeteen  and  over,  it  is  found  that 
only  11  of  the  cases  wdth  a  mitral  systolic  murmur,  or  15  per 
cent.,  occurred  in  the  yomiger  group,  whereas  of  the  107  patients 
in  the  older  group,  27,  or  25-2  per  cent.,  showed  the  presence 
of  a  mitral  systohc  murmur.  On  analysis  of  the  thirteen  cases 
where  the  apex  beat  was  outside  the  nipple  hne,  but  no  mitral 
systohc  murmur  was  present,  it  appears  that  seven  of  them  were 
in  the  younger  group  and  6  in  the  older ;  but  considering  the 
possibility  of  outward  rotation  of  the  apex  occurring  without 
any  actual  dilatation  of  the  left  ventricle  in  these  cases,  it  is 
preferable  to  rely  on  the  presence  of  a  murmur  rather  than 
on  the  position  of  the  apex  alone,  as  a  sign  of  left  ventricular 
failure. 

Cause  of  Eight  Ventricular  Dilatation  in  Anaemia 

In  the  next  place  the  cause  of  these  changes  in  the  shape 
and  size  of  the  heart  must  be  dealt  with. 

Is  it  secondary  to  failure  of  the  left  side  of  the  heart  ? 
The  first  question  to  be  asked  is  whether  in  anaemia  the 


242  AN.EMIA  OF  ADOLESCENCE 

cause  of  dilatation  of  the  right  ventricle  is  the  same  as  it  is 
in  valvular  disease  and  most  cases  of  overstrain,  where  its 
failure  is  secondary  to  that  of  the  left  ventricle. 

Some  light  upon  this  question  can  be  thrown  by  noting 
the  frequency  with  which  signs  of  left  ventricular  failure  are 
noticeable  in  cases  of  anaemia,  although,  as  already  pointed 
out  (p.  47),  these  signs  do  not  become  evident  clinically  unless 
well  marked. 

Still,  if  the  failure  we  are  now  speaking  of  were  secondary 
to  failure  of  the  left  side,  we  should  expect  to  find  that  every 
severe  case  of  failure  of  the  right  ventricle  showed  well-marked 
signs  of  failure  of  the  left  side. 

This  is,  however,  not  the  case,  as  the  following  statistics 
show ;  although  there  is,  as  might  be  expected,  more  frequently 
a  mitral  systolic  murmur  in  the  severe  than  in  the  slight  cases 
of  dilatation. 

Out  of  213  of  the  more  severe  cases  dealt  with,  an  apical 

systolic  murmur  was  only  noted  in  31  instances,  and  in  6  of 

these    it    was    only   a    faint    murmur.     In    only   3    cases   is 

•the  nmrmur  noted  as  being  loud  enough  to  be  conducted  to 

the  axilla. 

There  can,  however,  be  no  doubt  as  to  the  important  part 
which  a  failing  left  side  plays  as  a  rule  in  the  causation  of 
right  ventricular  dilatation,  although  in  the  cases  we  are  now 
dealing  with  the  part  it  plays  appears  to  be  only  a  very  minor 
one. 

It  is  possible  that  this  type  of  dilatation  is  secondary 
to  a  strong  rather  than  to  a  weak  left  ventricle,  because  a 
strong  left  ventricle  will  admit  of  far  more  physical  exertion 
than  would  be  possible  if  the  left  ventricle  were  weak. 

The  young  Avoman  whose  systemic  circulation  is  good 
will  work  till  she  is  stopped  by  the  breathlessness  which 
results  from  the  failure  of  her  right  ventricle.  The  patient  with 
a  weaker  left  ventricle  will  not  be  able  to  put  so  much  strain 
upon  her  right  heart  (see  illustrative  cases,  pp.  294  and  304). 

Secondly,  Is  the  failure  of  the  right  ventricle  due  to 
the  malnutrition  of  the  heart  muscle,  which  results  from  the 
anaemia  ? 


CAUSE  OF  CARDIAC  DILATATION  243 

The  answer  to  this  question  must  be  ui  the  affirmative, 
for  muscular  malnutrition  must  be  acknowledged  to  play 
some  part  in  causing  the  dilatation  we  are  deahng  with. 

As  has  already  been  pointed  out  (p.  10),  in  adolescence 
the  heart  depends  more  upon  its  muscular  than  upon  its 
fibrous  tissues  for  its  power  of  resisting  over- distension,  and, 
therefore,  any  weakening  of  the  power  of  its  muscles  by  malnu- 
trition must  tend  to  increase  its  habihty  to  dilatation  in  the 
face  of  any  undue  strain. 

A  weakly  lad  who  over- exerts  himself  is  more  apt  to  suffer 
from  cardiac  dilatation  than  a  stronger  one  is. 

That  malnutrition  of  muscular  tissues  does  occur  in  anaemia 
from  lack  of  oxygen,  and  possibly  also  of  other  nutritive 
materials  carried  by  the  blood,  is  sufficiently  self-evident 
not  to  need  further  comment  here. 

On  the  other  hand,  it  is  interesting  to  note  the  difference 
that  exists  between  the  tj'pe  of  ansBmia  w^e  are  here  discussing 
and  the  symptomatic  anaemia  which  is  second ar}^  to  some 
exhausting  disease  such  as  phthisis  or  nephritis.  In  such 
cases  it  seems  as  if  the  debility  which  accompanies  these 
conditions  so  far  weakens  the  heart  that  it  does  not  develop 
enough  interventricular  pressm'e  to  cause  marked  dilatation. 

This  is  clinically  so  certain  that  wdien  in  a  j^oung  woman 
a  considerable  amount  of  anaemia  is  unaccompanied  by  any 
upward  dilatation  of  the  right  ventricle,  it  is  safe  to  presume 
that  the  anaemia  is  secondary  to  some  organic  disorder  and 
is  not  a  simple  anaemia  which  will  be  curable  by  rest  and 
the  administration  of  iron. 

This  leads  up  to  the  next  point  to  be  considered — namel3% 
that  this  type  of  right  ventricular  dilatation  is  not  due  to 
muscular  malnutrition  alone,  but  that  another  factor  must 
be  recognised  as  well — namely,  '  overstrain.' 

Thirdly,  Oveistrahi  of  the  right  side  as  a  factor  in  causing 
dilatation  of  the  right  ventricle  in  anaemia. 

The  clinical  evidence  is  clear  that  overstrain  of  the  right 
ventricle  is  a  cause  of  its  dilatation  in  the  class  of  case  of 
which  we  are  now  speaking. 

Supposing  that  muscular  weakness  of  the  thinnest  part 

e2 


244  ANEMIA  OF  ADOLESCENCE 

of  the  muscular  wall  (owing  to  malnutrition)  were  the  sole 
cause  of  the  dilatation,  the  factors  causing  the  over-distension 
would  be  an  intraventricular  pressure  rather  less  than  normal 
'plus  a  wall  too  weak  to  withstand  it.  In  such  a  case,  although 
dilatation  would  occur,  the  work  done  by  the  muscular  con- 
traction would  not  be  in  excess  of  the  normal,  and  therefore 
the  heart  sounds  would  not  be  louder  than  normal.  Cases 
of  this  nature  are  sometimes  met  with  in  anaemia. 

In  the  case  of  ordinary  ansemic  dilatation,  on  the  other  hand, 
the  heart  sounds  are  usually  markedly  in  excess  of  the  normal, 
so  far  as  their  loudness  is  concerned,  and  also  the  character 
of  the  visible  and  palpable  pulsation  of  the  right  ventricle 
clearly  indicates  that  it  is  doing  more  work  than  it  does 
under  normal  circumstances.  Measurement  of  the  loudness 
of  the  second  sound  produced  by  the  closure  of  the  pulmonary 
valves  shows  clearly  that  the  pressure  closing  them  is  far 
above  the  average,  for  the  loudness  of  the  sound  is  sometimes 
double  what  it  is  in  health ;  for  if  the  normal  loudness 
of  the  pulmonary  second  sound  be  represented  by  the 
figures  16  to  20  or  so,  in  anaemic  dilatation  of  the  right 
ventricle  the  sound  frequently  measures  as  much  as  30  or 
40,  and  sometimes  as  much  as  48  (see  pp.  415  and  420,  '  Theory 
of  Compensation'). 

Further,  in  these  cases  the  sound  produced  by  the  closure 
of  the  pulmonary  valves  can  often  be  heard  distinctly  to  precede 
that  produced  by  the  aortic  valves,  causing  a  reduplication 
of  the  second  sound,  thus  proving  that  the  tension  in  the 
pulmonary  artery  is  in  excess  of  the  normal,  and  therefore 
causing  the  valves  to  close  earlier  than  usual. 

Both  of  these  observations  show  that  in  anaemic  dilatation 
of  the  heart  the  right  ventricle  is  developing  more  force  than 
normal,  and  that  therefore  overstrain  must  be  acknowledged  as 
a  factor  in  the  causation  of  the  dilatation.  As  already  pointed 
out  this  overwork  might  be  suspected  to  be  due  to  the  inter- 
ference with  the  pulmonary  circulation,  which  a  faihng  left 
ventricle  would  bring  about  Avere  it  not  that,  in  the  majority 
of  the  cases,  there  is  no  evidence  at  all  that  there  is  any  such 
failure. 

Moreover,  the  careful  measurement  of  the  loudness  of  the 


CAUSE  OF  CARDIAC  DILATATION  215 

pulmonary  second  sound  in  cases  of  valvular  disease,  where 
the  left  ventricle  is  failing,  shows  that  its  loudness  in  such  cases 
does  not  reach  the  extreme  degrees  which  it  does  in  cases  of 
anaemic  dilatation  of  the  heart. 

For  in  cases  of  failing  compensation  in  valvular  disease 
the  loudness  of  the  pulmonary  second  sound  would  only  be 
represented  by  the  figures  9  to  24,  and  very  rarely  as  much  as 
28  or  30  in  comparison  with  the  figures  of  30  and  40,  and  even 
48,  which  are  obtained  in  anaemia. 

These  observations  show  that  there  is  more  cause  for  embar 
rassment  of  the  right  ventricle  in  cases  of  anaemia,  than  the 
overstrain  which  results   from   failure   of  the  left   ventricle 
when  there  is  no  anaemia. 

Therefore,  the  statement  that  overstrain  is  a  factor  in  the 
causation  of  this  type  of  dilatation  of  the  right  ventricle  can 
not  only  be  confirmed,  but  also  exemplified  as  follows  : — 

The  dilatation  of  the  right  ventricle,  which  occurs  in  cases 
of  anaemia,  is  due  in  part  to  the  increased  work  which  is 
thrown  upon  the  right  ventricle  by  some  interference  with  the 
circulation  of  the  blood  through  the  limgs,  which  is  consequent 
upon  the  abnormal  condition  of  the  blood. 

While  observations  on  the  condition  of  the  heart  and 
circulation  in  cases  of  anaemia  show  the  presence  of  some 
hindrance  to  the  passage  of  the  anaemic  blood  through  the 
lungs,  there  is  no  evidence  at  present  to  show  upon  what 
the  cause  of  the  embarrassment  depends. 

The  natural  supposition  would  be  that  the  failure  in  the 
oxygen- carrying  power  causes  a  contraction  of  the  pulmonary 
venules,  so  as  to  keep  the  blood  in  contact  with  the  air  in 
the  lungs  for  as  long  a  time  as  possible  to  enable  the  blood 
to  take  up  the  maximum  of  oxygen  which  it  is  capable  of 
holding  ;  but  agamst  such  a  supposition  must  be  m'ged  the  fact 
that  physiologists  t^ll  us  that  they  know  of  the  existence  of  no 
such  regulating  mechanism  in  the  pulmonary  circulation. 

Nevertheless,  it  is  possible — in  this  case  as  in  some  other 
vital  phenomena — that  the  physiologist  must  learn  from  the 
clinician,  instead  of  the  physiologist  showing  the  way,  as  he 
usually  does. 

Another  alternative  is  that  there  may  be  an  increase  in  the 


246  ANiEMIA  OF  ADOLESCENCE 

total  volume  of  the  blood  in  these  anaemic  states,  and  that  in 
this  way  extra  work  is  thrown  upon  the  right  ventricle ;  and 
the  researches  made  in  this  direction  by  the  carbon  monoxide 
method  would,  if  confirmed,  give  some  weight  to  the  suggestion. 
This  cannot,  how^ever,  explain  all  cases,  for  it  is  quite  certain 
that  in  many  cases  of  anaemia  the  clinical  evidence  points  con- 
clusively to  the  total  volume  of  the  blood  in  active  circulation 
being  diminished  and  not  increased. 

It  is  quite  evident  that  further  research,  both  clinical  and 
experimental,  is  required  before  this  question  can  be  decided  ; 
and  most  interesting  results  would  be  obtainable  from  a  long 
series  of  cases  of  anaemia,  where  the  exact  loudness  of  the 
pulmonary  second  sound  was  carefully  noted  as  well  as  the 
loudness  of  the  pulmonary  murmur,  the  amount  of  cardiac 
dilatation,  and  the  level  of  the  diaphragm. 

I  regret  that  in  my  series  of  cases  the  loudness  of  the  pul- 
monary second  sound  and  the  level  of  the  diaphgram  w'ere  not 
accurately  noted,  and  therefore  I  am  unable  to  speak  definitely 
upon  the  varying  degree  of  resistance  to  the  pulmonary  circu- 
lation, which  was  present  in  them.  Neither  have  I  the  oppor- 
tunity of  collecting  another  group  of  cases,  because  observations 
such  as  these  upon  the  relative  loudness  of  the  heart  sounds 
cannot  be  spread  over  several  years,  owing  to  the  variation  in 
the  '  personal  equation  '  which  is  unavoidable  in  our  present 
method  of  measuring  the  loudness  of  the  cardiac  sounds. 
Such  observations,  to  be  fully  reliable,  ought  to  be  made  upon  a 
continuous  series  of  cases  seen  within  a  short  time — conditions 
which  are  afforded  by  hospital  out-patient  practice  in  a  manu- 
facturing town.  When,  however,  the  '  relay  telephone  '  can  be 
adapted  to  the  recording  mechanically  of  the  loudness  of  the 
heart  sounds,  many  of  these  prol)lems  will  be  dealt  with 
satisfactorily. 

In  what  has  just  been  said  as  to  the  important  part  which 
interference  with  pulmonary  circulation  plays  in  causing 
the  type  of  dilatation  of  the  right  ventricle,  which  is  now 
under  discussion,  it  is  not  intended  to  deny  the  part  which 
systemic  overstrain  may  play  in  these  cases. 

For  there  is  no  doubt  that  the  severity  of  the  cardiac 
failure  in  manv  of  the  cases  of  ana3mia,  with  which  we  are 


CAUSE  OF  CARDIAC  DILATATION  247 

dealing,  was  duo  to  the  fact  that  in  spite  of  weakness  and  mal- 
nutrition, the  ghl  had  to  continue  to  work  for  her  living  and 
often  at  work  requiring  consideraljle  exertion.  Where  the  heart 
was  weak,  owing  to  the  anaemia,  the  performance  of  ordinary 
work  would  result  in  overstrain  for  the  cardiac  muscle,  and  the 
result  would  be  much  the  same  as  that  produced  by  excessive 
work  upon  the  normal  heart  muscle. 

This  fact  will  be  made  clear  by  comparing  the  type  of 
dilatation  in  simple  overstrain,  apart  from  anaemia,  which  is 
described  in  Essay  VI,  p.  308,  with  the  type  of  dilatation  with 
which  we  are  now  dealing. 

Having  now  discussed  from  a  clinical  standpoint  the  nature 
of  the  dilatation  of  the  right  ventricle  which  occurs  in  anaemia, 
and  its  probable  cause,  the  subject  must  next  be  considered  from 
a  pathological  standpoint,  not  only  as  regards  the  alteration 
in  the  shape  of  the  ventricle  itself  and  its  effect  upon  adjacent 
structures,  but  also  as  regards  the  changes  in  the  circulation 
which  are  associated  therewith.  The  chief  of  these  changes 
is  that  wherein-  the  pulmonary  artery  systolic  murmur  is 
produced. 

The  theory  of  production  of  this  murmur  is  dealt  with  from 
the  pathological  side  in  the  follow-ing  essay,  w'hich  was  read 
l^efore  the  Pathological  Society  of  London  in  the  j^ear  1899, 
and  is  here  given  complete  as  it  appeal's  in  their  Transactions. 


Pathological  Aspects  of  Upw'aed  Dilatation  of  the 
Eight  Ventricle  ^ 

The  aim  of  this  paper  is  tw^ofold  :  firstly  to  demonstrate  the 
change  in  shape  which  the  upper  part  of  the  right  ventricle 
undergoes  when  it  dilates  ;  and  secondly,  to  show  the  changes 
in  the  pulmonary  artery  w-hich  result  from  this  upward 
dilatation  of  the  right  ventricle,  and  point  out  the  bearings 
which  they  have  upon  the  causation  of  the  systolic  murmur 
which  is  heard  over  the  pulmonary  artery  in  cases  of  cardiac 
overstrain  and  anaemic  dilatation  of  the  heart. 

1  Read  before  the  Pathological  Society  of  London,  April   18,  1899,  and 
reprinted  from  the  Tmnsadiovs  of  (he  Pathological  Society  of  London,  1899. 


Photographs  of  Caediac  Ventricles  from  Above  after  Removal  of  the 
Aorta,  Pulmonary  Artery,  and  the  Two  Auricles 


Fig.  59 — Normal  Heart. 

It  will  be  noticed  that  little  of  the 
anterior  wall  can  be  seen,  and  that  the  base 
of  the  pulmonary  artery  is  in  the  photo- 
graph almost  vertically  over  the  aortic 
valves. 


Fig.  60. — Heart  with  Slightly 
Dilated  Right  Ventricle. 

It  shows  that  the  anterior  wall  of  the 
right  ventricle  bulges  forward  in  front  of 
the  aorta,  and  pushes  the  origin  of  the 
pulmonary  artery  to  the  left  of  its  normal 
position. 


Fig.  61. — Heart  from  Aortic  and 
Mitral  Disease,  with  Dilata- 
tion and  Hypertrophy  of 
BOTH  Left  and  Right  Ven- 
tricles. 

It  shows  very  marked  forward  bulging 
of  the  anterior  wall  of  the  right  ventricle 
and  the  considerable  displacement  of  the 
pulmonary  artery  to  the  left.  It  also  shows 
that  the  pulmonary  valves  and  upper  part 
of  the  right  ventricle  are  not  in  the  plane 
of  the  auriculo-ventricular  septum  as  in 
Figs.  59  and  GO,  but  he  in  a  higher  plane 
— i.e.  are  m  the  photograph  projecting 
forwards  towards  the  obsers'er. 


Fios.  G2  AKD  63. — Lateral  View  of  Distended  Hearts.    (Drawn  from 
photographs,  three-sevenths  natural  size.) 


7'  ^ 

Fig.  62. — Normal  Heart. 


Fig.  63. — Heart  with  Slight 
Dilatation  of  the  Right 
Ventricle  Upwards. 

It  shows  the  elevation  of  the  puimonary 
valves  and  ccnsequent  shortening  of  the 
artery,  and  also  the  altered  direction  of 
tlio  artery  relatively  to  the  main  axis  of 
the  right  ventricle. 


Fig.  64. — Semi-diagrammatic  View 
of  a  Normal  Heart  as  seen 
IN  Section  throvgh  the 
Pulmonary  Artery  and 
Right  Ventricle. 

To  illustrate  the  shortening  and  dilata- 
tion of  the  pulmonary  artery  which  results 
from  upward  dilatation  of  the  right 
ventricle.  The  dotted  line  represents  the 
change  that  takes  place. 


250  UPWARD  DILATATION  OF  HEART 

This  paper  is  illustrated  by  the  study  of  three  hearts  : — 

1.  From  a  man  who  died  as  the  result  of  an  accident.  This 
heart  may  be  considered  normal. 

2.  From  a  woman,  aged  forty-eight,  who  died  suddenly 
from  hemiplegia  wdth  cardiac  failure,  and  who  was  found  to 
have  a  congenital  defect  in  the  interauricular  septum.  In 
this  case  the  right  ventricle  and  right  auricle  are  rather 
dilated,  and  the  left  are  approximately  normal. 

3.  From  a  girl  aged  fifteen,  who  died  from  cardiac  failure, 
the  result  of  disease  of  both  aortic  and  mitral  valves.  In  this 
case  the  right  ventricle  is  greatly  dilated  as  well  as  the  left 
ventricle  and  auricle. 

The  hearts  were  distended  with  hard  paraffin  prior  to  their 
removal  from  the  body,  with  the  exception  of  that  from 
Case  II,  fig.  60,  which  was  not  distended  in  situ. 

As  to  the  pressure  under  wdiich  the  injection  w^as  made, 
I  employed  an  ordinary  injection  syringe  and  did  not  use  a 
manometer  or  other  pressure  gauge,  but  was  careful  not  to  over- 
distend  the  hearts.  I  cannot,  therefore,  state  the  pressure 
employed,  nor  do  I  consider  it  a  point  of  importance  in  the 
present  connection,  since  my  object  is  to  illustrate  one  of  the 
ways  in  which  the  ventricle  dilates,  and  not  the  degree  of 
dilatation  that  occurs.  I,  nevertheless,  am  confident  that  the 
specimens  which  I  am  showing  are  truthful  in  this  respect  also. 

Figs.  59  to  61  show  the  ventricles  isolated  by  the  removal 
of  the  auricles  and  aorta  and  pulmonary  artery. 

Comparison  of  the  two  dilated  right  ventricles  thus  isolated, 
with  that  of  the  normal  heart  shows  very  clearly  the  change 
in  shape  which  takes  place  when  the  right  ventricle  dilates 
upwards  in  the  manner  so  well  described  by  Dr.  Foxwell  in  his 
'  Essays  on  Heart  and  Lung  Disease.' 

In  a  view  of  the  isolated  ventricles  from  above,  as  in  the 
photographs  (figs.  59,  60,  and  61),  the  dilated  upper  portion  of 
the  right  ventricle  is  seen  as  a  distinct  prominence  bulging 
forwards  beyond  the  normal  limits.  Not  only  does  it  project 
anteriorly,  as  is  well  shown  in  the  photographs  of  hearts,  figs. 
60  and  61,  but  it  also  projects  upwards  beyond  the  plane  of 
the  auriculo-ventricular  septum,  and  so  comes  to  overhang  the 
commencement  of  the  aorta.     This  was  well  seen  in  the  case 


PATHOLOGICAL  A8PECTR  251 

of  the  heart  shown  in  fig.  61 ,  when  the  isolated  ventricle  was 
viewed  from  the  side.     It  can  be  seen  in  fig.  61. 

I  do  not  show  these  specimens  of  upward  dilatation  of  the 
right  ventricle  as  an  unusual  condition,  but  as  good  demon- 
stration of  a  very  common  condition  ;  for  although  this  type 
of  dilatation  seems  to  be  but  seldom  referred  to  in  current 
literature,  I  believe  that  if  it  be  carefully  looked  for  clinically 
and  in  the  post-mortem  room  it  will  be  found  to  be  extremely 
frequent  in  cases  of  cardiac  failure  from  a  great  variety  of 
causes. 

It  is,  I  l)elieve,  the  ordinary  type  of  dilatation  in  youth  and 
early  adult  life,  for  at  this  period  dilatation  of  the  right  ventricle 
upwards  and  to  the  left  usually  precedes  and  exceeds  in  amount 
any  dilatation  of  the  ventricle  to  the  right. 

In  adults  this  upward  dilatation  seems  to  be,  as  a  rule, 
less  marked  than  dilatation  to  the  right  of  the  sternum,  and 
after  the  age  of  forty-five  or  so  it  seems  to  be  decidedly  rare  ; 
for  in  the  later  years  of  hfe,  the  dilatation  is  towards  the  right 
side,  and  the  conus  arteriosus  yields  but  little. 

The  upward  dilatation  is  often  very  extreme  in  youth  and 
adolescence.  For  example,  the  relative  dullness  of  the  heart, 
shown  in  fig.  61,  commenced  above  the  second  rib  on  the  left  side 
and  extended  to  the  nipple  line  in  the  third  left  interspace,  and 
after  death,  some  months  subsequently,  the  pulmonary  valves 
were  found  to  lie  at  the  level  of  the  first  rib.  Such  a  degree 
of  dilatation  is  not  very  uncommon. 

I  now  come  to  the  consideration  of  the  effect  which  this 
upward  extension  of  the  conus  arteriosus  has  upon  the 
pulmonary  artery.  Its  effect  is  twofold  :  firstly,  the  artery 
is  shortened  ;    secondly,  the  direction  of  its  course  is  altered. 

Firstly,  as  to  the  shortening  of  the  pulmonary  artery. 
It  is  evident  that  the  increase  of  the  upper  part  of  the  right 
ventricle  upwards  and  to  the  left  must  carry  the  origin  of  the 
pulmonary  artery  upwards  with  it ;  and  since  the  course  of  the 
artery  is  normally  upwards  from  the  pulmonary  valves,  any 
elevation  of  the  point  of  origin  must  shorten  the  course  of  the 
artery.  This  is  shown  by  comparing  fig.  62  with  fig.  63,  and 
also  by  the  diagram. 

When,  as  is  often  the  case,  the  pulmonary  valves  lie  under 


252  UPWARD  DILATATION  OF  HEART 

the  second  rib  instead  of  under  the  third,  this  shortening  must 
amount  to  f  inch  or  more,  leaking  the  normal  length  of  the 
artery  at  2|  inches,  this  would  mean  a  shortening  of  30  per  cent. 
The  effect  of  this  shortening  must  be  to  relax  the  walls  of  the 
artery. 

This  relaxation  may  be  seen  post-mortem  as  a  distinct 
wrinkling  of  the  arterial  wall  in  extreme  cases  (see  fig.  63). 
More  often,  however,  the  elastic  contractility  of  the  vessel 
prevents  any  distinct  wrinkling.  Although  the  relaxation 
of  the  vessel  wall  may  not  show  after  death  when  the  artery 
is  empty,  it  cannot  fail  to  cause  some  distortion  during  life. 
The  relaxed  wall  is  sure  to  yield  abnormally  to  the  blood  pressure, 
and  dilatation  of  the  artery  will  result.  There  will,  therefore, 
be  both  shortening  and  dilatation  of  the  pulmonary  artery, 
and  the  two  combined  will  tend  to  make  the  artery  become 
more  spherical  than  normal.  In  other  words,  when  the  short- 
ening is  considerable,  there  will  be  an  aneurysmal  bulging  of 
the  pulmonary  artery  under  the  influence  of  the  blood  pressure. 

And  now  as  to  the  altered  direction  of  the  ^pulmonary  artery. 
Taking  the  normal  course  of  the  first  part  of  the  artery  as  being 
obliquely  upwards  and  backwards,  it  is  evident  that  if  its 
point  of  origin  is  raised  its  course  will  become  more  horizontal 
than  normal.  When,  as  often  happens,  the  pulmonary  valves 
lie  under  the  second  rib  instead  of  under  the  third,  the  alteration 
in  the  course  of  the  artery  is  considerable. 

This  altered  course  means  an  alteration  in  the  axis  of 
the  pulmonary  artery  as  compared  with  the  axis  of  the 
ventricle,  and  instead  of  the  artery  being  fairly  in  line  with 
that  axis,  as  it  ought  to  be,  it  will  be  at  an  angle  to  it.  I 
have  frequently  noted  this  change  in  the  direction  of  the 
pulmonary  artery,  post-mortem,  more  especially  if  the  ventricle 
happened  to  be  distended.  Under  such  circumstances  the 
sudden  dipping  backwards  of  the  artery  is  most  noticeable. 
Thus,  in  the  case  of  the  heart  shown  in  fig.  61,  I  noted  at 
the  post-mortem  that  the  first  part  of  the  pulmonary  artery 
was  at  right  angles  to  the  longitudinal  axis  of  the  right  ventricle, 
instead  of  being  nearly  in  the  same  line  as  in  a  normal  heart. 

In  fig.  64,  a  semi-diagrammatic  view  is  given  of  a  section 
through  the  centre  of  the  pulmonary  artery  and  right  ventricle 


PATHOLOGICAL  ASPECTS  253 

to  illustiate  the  distortion  of  the  former.  It  is  not  easy  to 
represent  the  change  in  the  direction  of  the  artery  of  which 
we  are  now  speaking  in  this  diagram,  because  it  is  accompanied 
by  a  movement  of  the  pulmonary  artery  and  valves  to  the  left  of 
the  normal  position — i.e.  out  of  the  plane  of  the  diagram.^ 

This  lateral  movement  of  the  artery  is  well  shown  in  the 
photographs  on  p.  248.  In  the  normal  heart  (fig.  59),  the 
pulmonary  valves  are  seen  to  be  almost  vei-tically  over  the 
aortic  valves.  In  both  of  the  other  hearts  the  pulmonary 
valves  and  base  of  the  pulmonary  artery  are  seen  to  lie 
considerably  to  the  left  of  their  normal  position. 

The  practical  result  of  this  alteration  in  the  direction  of 
the  pulmonary  artery  as  compared  with  the  axis  of  the  ventricle, 
is  as  follows  :  When  the  ventricle  contracts,  the  blood  is 
thrown  against  the  anterior  wall  of  the  pulmonary  artery, 
instead  of  being  thrown  in  the  direction  of  its  lumen.  This 
will  be  seen  on  comparing  fig.  62  with  fig.  63. 

Here,  then,  we  have  two  conditions  eminently  favom'able 
to  the  production  of  an  aneurysmal  murmur.  We  have  a 
pulmonary  artery  that  becomes  more  globular  than  normal 
under  the  influence  of  the  blood  pressure,  and  we  have  the 
blood  thro\\Ti  into  it  so  as  to  strike  one  of  its  walls — conditions 
likely  to  bring  about  a  murmur-producing  eddy  in  the  dilated 
artery. 

These  two  factors,  the  increased  distensibility  of  the  pul- 
monary artery,  and  the  alteration  of  its  axis,  as  compared 
with  that  of  the  right  ventricle,  are,  I  believe,  of  prime 
importance  in  the  causation  of  the  common  systolic  murmur 
which  is  audible  over  the  second  left  interspace  in  cases  of 
cardiac  overstrain  and  cardiac  debility  in  anaemia  and  other 
diseases  :  in  other  words,  I  feel  satisfied,  from  clinical  and 
pathological  evidence — to  which  I  cannot  refer  within  the 
limits  of  this  paper — that  the  type  of  dilatation  of  the  right 
ventricle  with  which  this  paper  deals  is  the  pathological  con- 
dition which  produces  the  common  pulmonary  systolic  murmur 

^  The  attachment  of  the  posterior  part  of  the  pulmonary  artery  and  of 
the  adjacent  part  of  the  right  ventricle  to  the  anterior  part  of  the  aorta  and 
left  ventricle  is  not  suflficiently  firm  to  prevent  such  a  shifting  of  the  pulmonary 
artery  from  taking  place. 


25 1  AN.^MIA  OF  ADOLESCENCE 

of  anaemia  and  overstrain,  ami  that  the  mechanism  is  such  as 
I  have  suggested. 

I  do  not  say,  however,  that  upward  dilatation  is  sufficient 
by  itself  to  produce  this  murmur  in  all  states  of  the  circulatoin, 
for  I  know  that  such  is  not  the  case.  Extreme  degrees  of 
upward  dilatation  of  the  right  ventricle  can  exist  without 
producing  any  basal  murmur  {vide]).  314  and  fig.  118). 

Upward  dilatation  of  the  ventricle  does,  however,  give  rise 
to  the  possibility  of  an  aneurysmal  murmur  being  produced 
in  the  pulmonary  artery. 

When  the  conditions  of  the  circulation  are  favourable,  an 
aneurysmal  murmur  is  produced  in  the  artery,  and  even  an 
aneurysmal  thrill.  When  they  are  not  favourable  no  murmur 
will  be  produced. 

This,  then,  is  the  bearing  which  I  believe  upwtird  dilatation 
of  the  right  ventricle  has  upon  the  production  of  the  pulmonary 
systolic  murmur  of  anaemia  and  cardiac  debihty. 

Having  discussed  the  pathological  changes  which  are 
noticeable  in  anaemic  heart  failure,  and  the  theory  which  they 
suggest  as  to  the  cause  of  the  htiemic  murmur  which  is  heard 
in  these  cases,  the  clinical  character  of  this  murmur  must  now 
be  discussed  in  some  detail  in  order  full}^  to  test  the  applica- 
bility of  the  theory  which  has  been  propounded  as  to  its 
origin  in  a  dilated  pulmonary  artery. 

Pulmonary  Artery  Systolic  Murmur 

In  the  first  place,  this  murmur — which  was  formerly  called 
the  basal  luemic  murmur  of  anaemia — must  be  defined.  It  is 
a  systolic  murmur  heard  at  the  base  of  the  heart  in  cases  of 
anaemia  with  heart  failure,  and  its  point  of  maximal  loudness 
is  usually  in  the  second  interspace  to  the  left  of  the  sternum 
and  over  the  situation  of  the  origin  of  the  pulmonary  artery. 

Its  Frequency. — In  anaemia  this  pulmonary  murmur 
is  heard  in  the  majority  of  cases  wdiich  show  signs  of  cardiac 
failure.  The  actual  figures  obtained  from  the  series  of  cases 
here  dealt  with  are  as  follows  : — 

Out  of  350  consecutive  cases  of  anaemia,  in  63  no  notes 


PULMONAEY  SYSTOLIC  MURMUR  255 

were  taken,  and  in  45  the  heart  was  normal,  leaving  242 
cases  of  heart  failure  of  which  notes  were  taken. 

Out  of  these  242  cases  8  are  not  available,  as  no  note 
was  made  as  to  the  presence  or  absence  of  a  pulmonary 
murmur.  Out  of  the  remaining  234  cases  a  pulmonary 
murmur  was  present  in  227  instances,  or  exactly  97  per  cent, 
of  the  cases. 

It  can  therefore  be  asserted  that  a  pulmonary  artery 
systolic  murmur  is  usually  present  in  cases  of  the  heart  failure 
which  accompanies  the  simple  anaemia  (and  chlorosis)  of 
adolescence. 

The  clinical  features  of  this  murmur  will  now  be  discussed 
under  the  headings  : — 

Its  character  :  '  What '  is  it  ? 

Its  time  relationships  :   '  When  '   is  it  heard  ? 

Its  point  of  maximal  loudness  and  area  of  audition  : 
•  Where  '  is  it  heard  ? 

The  factors  at  work  in  its  causation  :  '  How  '  is  it  produced  ? 

The  Character  of  the  pulmonary  systolic  murmur. — 
This  murmur  is  usually  somewhat  low  in  tone,  and  resembles 
a  faint  aneurysmal  murmur  more  closely  than  it  does  the 
higher  pitched  and  more  blowing  murmur  of  mitral  regurgita- 
tion. As  regards  its  loudness  it  shows  a  wide  range,  for  not 
only  does  its  loudness  in  any  particular  case  vary  very  readily 
with  changes  in  the  heart's  activity,  and  even  with  the  attitude 
the  patient  is  in  during  auscultation,  but  it  also  shows  a  wide 
range  of  loudness  according  to  the  severity  of  the  anaemia 
present.  In  a  slight  case  the  murmur  may  be  soft,  low-toned, 
and  barely  audible ;  and  in  a  more  severe  case  it  may  be  so 
loud  as  to  be  heard  over  the  greater  part  of  the  chest  and  even 
be  accompanied  by  a  w^ell-marked  vibratile  thrill  such  as  that 
felt  over  an  aneurysm. 

Moreover,  a  murmur  of  this  degree  of  intensity  may  be  fomid 
to  disappear  entirely  in  a  few  weeks,  coincidently  with  the 
general  improvement  of  the  patient. 

This  fact  of  the  ready  variabihtj'-  of  the  miumur  and 
that  it  does  not  occur  in  any  particular  case  with  the  com- 
paratively  regular   loudness   which   we   associate   with   such 


256 


AN.EMIA  OF  ADOLESCENCE 


systolic  murmurs  as  those  produced  at  the  mitral  or  aortic 
orifices  is  of  very  considerable  importance. 

Variability  of  the  pulmonary  systolic  murmur  with 
Change  of  Attitude  of  the  patient. — This  is  one  of  the  most 
marked  features  of  this  murmur. 

Often  when  the  murmur  is  faint  or  almost  inaudible  when 
the  patient  is  standing  it  becomes  quite  distinct  or  even  loud 
on  lying  down  (see  figs.  65  and  66).     It  is  the  rule  that  this 

Case  SHO-rnxG  Loud  Pulmonary  Murmur  when  Recumbext  and  xo 
Murmur  when  Erect 


Fig.  65. 

Eliza  C,  age^l  twenty- 
three,  March  31,  1891. 
Showing  normal  heart  in 
erect  attitude.  No  dilatation 
and  no  murmur. 


Area,  of 
audition,  of 
j)uJmoiia,T^ 
jtziiLnnizr 


Fig.  66. 

Ehza  C,  March  31,  1891.  Showing  upward  dis- 
placement and  dilatation  of  the  heart  on  lying  down, 
with  a  loud  pulmonary  murmur  audible  into  vessels 
of  the  neck,  also  IJ  inches  of  dullness  in  second  left 
space  and  a  systolic  murmur  at  the  apex. 


murmur  is  distinctly  louder  when  the  patient  is  Ij^ing  down 
than  it  is  when  sitting  up  or  standing.  Statistics  on  this 
point  are  as  follows  :  In  fifty-two  cases  where  this  murmur 
was  audible,  the  effect  of  change  of  the  patient's  position  was 
noted,  with  the  result  that  in  forty-seven  instances  the  murmur 
was  distinctly  louder  when  the  patient  was  recumbent.  In 
three  cases  there  was  no  definite  change  and  in  two  cases  the 
murmur  was  distinctly  louder  when  the  patient  was  in  the 
erect  attitude. 

These  two  cases  were,  however,  exceptional  in  other  ways, 
and  will  be  dealt  with  later  on  (uide  p.  300). 

Thus  in  96  per  cent,  of  the  cases  examined  in  this  series 
the  murmur  was  increased  in  loudness  in  the  recumbent  attitude, 


PULMONARY  SYSTOLIC  MURMUR  257 

and  this  statement  quite  coincides  with  what  is  usually  found 
when  this  murmur  is  hstened  for  in  these  two  different  attitudes. 
This  question  is  again  referred  to  below  {nide  p.  266). 

Variability  with  slight  changes  in  the  heart's  activity. — ■ 
Fm-ther,  the  increase  in  the  loudness  of  the  mm-mur  when 
the  heart  is  acting  excitedly  is  somewhat  in  excess  of  that 
usually  observed  in  the  case  of  other  cardiac  murmurs,  under 
similar  circumstances.  Nervous  excitement,  too,  will  increase 
this  murmur  more  than  it  will  increase  organic  cardiac  murmurs. 
These  facts  must  be  borne  in  mind  when  testing  the  effect 
of  change  of  attitude  ;  for  the  exertion  of  sitting  up  or  walking 
to  a  couch  and  lying  down  will  in  some  cases  decidedly  increase 
the  loudness  of  the  murmur  for  some  few  seconds  (for  illustra- 
tion, vide  p.  268). 

Again,  if  the  loudness  of  the  murmur  be  carefully  noted, 
and  especially  if  some  means  be  used  for  testing  its  power 
of  penetration  through  some  resisting  medium  {vide  p.  413),  it 
will  often  be  found  that  there  is  a  shght  respiratory  variation 
in  its  loudness,  and  that  the  mm-mur  with  the  cardiac  beat 
occurring  at,  or  just  after,  the  end  of  inspiration  is  a  httle 
louder  than  the  murmur  occurring  with  the  beats  during 
the  remainder  of  the  respiratory  cycle. 


e> 


Time  and  Mode  of  Occurrence  of  the  pulmonary  systoUc 
murmur. — The  murmur,  as  its  name  imphes,  is  systohc  in 
rhythm,  accompanying  but  not  replacing  the  first  sound  of 
the  heart,  although,  when  at  all  loud,  it  may  seem  to  do  so. 

When  the  murmur  appears  to  replace  the  first  sound  at 
the  base  of  the  heart,  it  will  be  found,  nevertheless,  on  listem'ng 
lower  down,  over  the  fourth  and  fifth  interspaces,  that  as 
the  murmur  lessens  in  loudness  the  first  sound  becomes  more 
distinct,  until  a  point  may  usually  be  found,  towards  the  lower 
end  of  the  sternum,  where  the  right  ventricular  first  somid 
may  be  heard  pure  and  free  from  murmur. 

If  it  were  possible  to  record  the  exact  time  of  occurrence 
of  the  murmur,  it  would,  I  feel  sure,  be  found  to  begin  a 
fraction  of  a  second  later  than  the  commencement  of  a 
systohc  regurgitant  murmur. 

s 


258  ANiEMIA  OF  ADOLESCENCE 

The  characteristic  of  the  murmur  to  be  next  discussed  is  the 
place  or  area  where  it  is  heard. 

Point  of  Maximal  Intensity,  Area  of  Audition  and 
Direction  of  Conduction  of  the  pulmonary  systolic  murmur. 
— The  point  of  maximal  intensity  of  the  murmur  is  usually 
found  to  be  at  the  sternal  end  of  the  second  left  interspace. 
Its  exact  position  varies  somewhat  in  different  cases,  and  this 
variation  is  apparently  due  to  the  fact  that  the  murmur  is 
best  heard  over  the  situation  of  the  pulmonary  valves  and 
the  adjacent  part  of  the  pulmonary  artery,  and  the  position  of 
these  structures  is  not  constant,  but  is  found  to  vary  according 
to  the  amount  of  dilatation  of  the  right  ventricle  which  is 
present  in  any  particular  case.  In  some  cases  the  pulmonary 
valves  lie  close  to  their  normal  situation  under  the  sternal 
end  of  the  third  costal  cartilage.  Whereas,  when  there 
is  much  upward  dilatation  of  the  ventricle,  they  may  lie  in 
the  second  left  interspace  as  much  as  one  inch  or  more  away 
from  the  sternum.  Also  they  may  lie  at  a  much  higher  level 
than  normal  and  be  under  the  second  rib  or  even  higher. 
Under  such  conditions  the  point  of  maximal  intensity  of  the 
murmur  (or  the  '  P.M.I.,'  as  it  may  be  called)  will  be  corre- 
spondingly farther  from  the  sternum  or  higher  than  normal. 
Practically,  it  will  be  found  that  the  P.M.I,  of  the  murmur 
is,  as  a  rule,  the  same  as  the  P.M.I,  of  the  pulmonary  second 
sound. 

As  regards  the  situation  of  the  P.M.I,  of  the  murmur,  it 
can  sometimes  be  noted  that  it  changes  a  little  with  the  change 
in  the  amount  of  the  cardiac  dullness  in  the  second  interspace, 
which  takes  place  when  the  patient  lies  down. 

It  may  not  infrequently  be  noticed  that  the  P.M.I,  of  the 
pulmonary  second  somid  is  definitely  at  a  higher  level  in 
the  recumbent  than  in  the  erect  attitude,  and  occasionally 
this  same  observation  may  be  made  with  the  less  easily 
definable  point  of  maximal  intensity  of  the  pulmonary 
systolic  murmur. 

The  Area  of  Audition  of  the  murmur. — The  size  of  the 
area  over  which  the  murmur  can  be  heard  depends,  naturally, 
upon  the  loudness  of  the  murmur. 


PULMONARY  SYSTOLIC  MURMUR  259 

When  faint,  its  area  of  audition  is  only  that  of  a  half-crown 
or  five-shiUing  piece,  and  is  situated  just  over  the  pulmonary 
valves  ;  when  louder,  the  area  extends  upwards  and  to  the  left 
towards  the  centre  of  the  clavicle,  and  is  elliptical  in  shape 
{vide  fig.  71,  p.  620;. 

A  point  of  importance  is  that  the  murmur  is  not  well 
heard  below  the  fourth  rib  unless  it  be  very  loud.  If,  when 
the  murmur  is  not  well  conducted  elsewhere,  it  appears  to 
be  heard  just  to  the  left  of  the  sternum  in  the  third,  fourth, 
and  fifth  interspaces,  it  may  be  taken  for  granted  that  what 
appears  to  be  a  propagation  downwards  of  the  pulmonary 
systolic  murmur  is  really  due  to  the  presence  of  a  tricuspid 
regurgitant  murmur,  and  is  not  a  sign  that  the  pulmonary 
artery  murmur  is  audible  over  these  interspaces. 

When  the  pulmonary  murmur  is  loud  it  may  have  a  fairly 
wide  area  of  audition  downwards  as  well  as  on  both  sides 
of  the  sternum,  and  an  exceptionally  loud  murmur  may  be 
audible  over  the  whole  of  the  upper  part  of  the  chest  and  the 
cardiac  region.  There  is  one  point  of  diagnostic  importance 
to  be  noticed  with  regard  to  the  conduction  of  this  murmur 
and  that  is  that  when  the  murmur  is  loud  it  may  be  conducted 
into  the  carotid  and  subclavian  arteries  and  so  cause  doubt 
as  to  whether  a  true  aortic  systohc  murmur  be  present  or 
not. 

When  a  thrill  is  present  it,  too,  may  be  just  palpable  in 
the  carotid  arteries.  The  reason  for  this  direction  of  conduc- 
tion is  to  be  found  in  the  anatomical  relationship  of  the 
pulmonary  artery  and  the  aorta.  If  this  be  studied  it  wall 
be  seen  that  if  the  pulmonary  artery  were  to  be  distended 
and  altered  in  position  so  as  to  he  somewhat  higher  than 
normal  it  would  come  into  close  relationship  with  the  inner 
side  of  the  upper  part  of  the  ascending  arch  of  the  aorta  and 
of  the  commencement  of  the  transverse  arch.  It  can  therefore 
easily  be  understood  that  when  the  blood  in  the  distended 
pulmonary  artery  is  vibrating  sufficiently  to  cause  a  loud 
murmur,  or  even  the  palpable  thrill  that  can,  in  exceptional 
cases,  be  felt,  these  vibrations  must  involve  that  part  of  the 
aorta  against  which  the  pulmonary  artery  is  pressed  and  by 
throwing  the    blood  in  the  aorta  into  vibration  lead  to  the 

s2 


Pulmonary  Murmur  and  Upward  Dilatation  of  Right  Ventricle,  both 
Moderate.  (Area  of  Audition  of  the  Murmur  shown  by  dotted 
Shading.) 


Ptdmonar, 
murmur 


Fig.  67. 
Nellie  H.,  aged  nineteen. 


Fig.  68. 

Sarah  J.,  aged  twenty. 
Faint  murmur. 


Fig.  69. 

Jane  T.,  aged  seventeen. 
Murmur  very  faint. 


Fig.  70. 

Eose  K  ,  aged  fifteen. 


Fig.  71. 

Minnie  P.,  aged  sixteen. 
Murmur  moderately  loud. 
Right  ventricle  third  sound 
present.  When  erect,  first  sound 
1  ouder ;  pulmonary  murmur 
fainter. 


Fig.  72. 

Annie  D.,  aged  sixteen.  Pul- 
monary murmur  moderately 
loud.  Pamt  mid-diastoUc  mitral 
present. 


PULMONARY  SYSTOLIC  MURMUR 


261 


Loud  Ptjlmonaby  Murmur  with  Considerable  Dilatation,  and  Figs.  73, 
74,  AND  76  with  Functional  Mitral  and  Tricuspid  Murmurs  as  well 

Pulmonary 
rnu^rniur    1 


Fig.  73. 

Gertrude  L.,  aged  nineteen. 
Loud  pulmonary  also  mitral 
and  tricuspid  murmurs.  Wlien 
erect,  no  tricuspid  and  a  fainter 
pulmonary  murmur. 


Fig.  74, 

Jane  B.,  aged  twenty. 
Loud  pulmonary  and  mitral 
murmurs  and  faint  tricuspid. 


conducted  to  vessels  of 
the  neck 


^=^ext.KZ. 


Pujr 


Tricusp. 
xaurm. 


Fig.  75. 

Ellen  H.,  aged  twenty.  Consider- 
able dilatation  and  loud  and  widely 
conducted  pulmonary  murmur.  After 
a  few  weeks'  treatment  the  heart  was 
normal  again. 


Fig.  76. 

Eliza   E.,   aged  nineteen.  Great 

dilatation ;    loud    pulmonary,  sharp 

blowing   tricuspid,  and    soft  mitral 
murmurs. 


conduction  of  the  mui*mur  along  the  arteries.  Careful  examina- 
tion will  confirm  this  theory  as  to  the  arterial  conduction  of 
the  pulmonary  systolic  mm-mm-,  for  it  will  be  noticed  that 
the  mm-mm-  is  rather  better  heard  in  the  left  carotid  and  sub- 
clavian arteries  than  it  is  in  the  right.  This  appears  to  be  due 
to  the  fact  that  the  vibrations  coming  from  the  pulmonary 
artery  are  not  so  likely  to  involve  the  blood  passing  up  the 
innominate  artery  as  they  are  the  blood  which  remains  a  little 


262  ANEMIA  OF  ADOLESCENCE 

longer  in  the  arch  of  the  aorta  and  comes  more  in  contact 
with  that  part  of  the  vessel  against  which  the  vibrating 
pulmonary  artery  is  pressed. 

Figs.  67  to  76,  taken  from  my  out-patient  case-books, 
show  the  variations  in  the  area  of  audition  and  direction  of 
conduction  of  this  murmur  in  different  cases. 

Having  discussed  the  chief  characteristics  of  this  murmur, 
the  theoretical  consideration  as  to  its  mode  of  production 
must  now  be  taken  up. 

Before  doing  so,  however,  I  must  say  a  few  words  as  to 
the  important  work  which  the  late  Dr.  Arthur  Foxwell  did 
upon  this  subject.  Those  who  compare  what  I  have  here 
written  upon  the  heart  in  anaemia  with  his  published  writings 
will  see  that  I  am  travelling  upon  much  the  same  lines  that 
he  did.  It  was  his  work  which  stimulated  me  twenty-five 
years  ago  to  devote  much  of  my  time  to  this  subject,  and 
much  of  what  I  am  now  writing  consists  in  filling  in  the  main 
outlines  of  the  subject  which  were  sketched  out  by  him. 

As  regards  the  cause  of  the  pulmonary  systolic  murmur, 
I  am  partly  in  agreement  with  him  and  partly  not. 

As  regards  the  part  played  by  relaxation  of  the  wall  of 
the  pulmonary,  I  can  fully  confirm  all  he  said,  but  I  do  not 
consider  that  the  other  factor  he  spoke  of  is  so  important  as 
he  seemed  to  think  :  I  refer  to  the  alteration  in  level  of  the 
valve-plane  in  the  pulmonary  artery.  In  the  undistended 
heart  post-mortem,  it  is  certainly  noticeable  that  the  anterior 
portion  of  the  pulmonary  valve  lies  at  a  higher  level  than 
its  posterior  part.  And  I  have  seen  a  case  where  the  top  of 
the  anterior  cusp  of  the  valve  was  under  the  upper  border 
of  the  first  rib,  whereas  the  top  of  the  posterior  cusp  was  under 
the  lower  border  of  the  same  rib.  This  would  seem  to  confirm 
Dr.  Foxwell's  view.  When,  however,  such  a  heart  as  this  is 
distended,  it  is  found  that  this  alteration  in  the  plane  of  the 
valve  is  simply  due  to  the  altered  direction  of  the  artery,  and 
as  the  valve  is  still  at  right  angles  to  the  direction  of  the  blood- 
fiow  there  is  nothing  in  this  alteration  likely  to  cause  a  murmur. 

In  this  connection  it  is  interesting  to  note  that  the  union 
between  the  posterior  wall  of  the  pulmonary  artery  and  the 


PULMONARY  SYSTOLIC  MURMUR  263 

anterior  wall  of  the  aorta  is  not  very  firm  in  these  cases,  and 
that  the  relative  position  of  the  two  orifices  is  capable  of  a 
certain  amount  of  variation  {vide  p.  253,  and  figs.  60,  61). 

Mode  of  Production  of  the  pulmonary  systolic  murmur. — 
The  various  chnical  characteristics  of  this  murmur  must  now 
be  reviewed  in  connection  with  the  theory  as  to  its  production 
already  advanced — namely,  that  it  is  a  mm-mur  produced 
during  systole  in  an  anemysm-hke  over-distension  of  the 
pulmonary  artery  which  is  rendered  possible  by  the  relaxation 
of  its  walls,  brought  about  by  the  upward  dilatation  of  the 
conus  arteriosus  of  the  right  ventricle. 

1.  The  murmur  is  evidently  a  right  ventricle  murmur 
and  not  a  left  ventricle  one.     This  is  shown — 

(1)  By  its  ready  variability — 

(a)  With  change  in  the  attitude  of  the  patient  as  already 

pointed  out  (p.  256)  ; 
(fe)  With  shght  changes  in  the  strength  of  the  heart's 

action — e.g.  on  excitement  and  slight  exertion  and 

with  respiration  ;  and — 

(2)  Its  right  ventricular  origin  is  also  suggested  by  its 
lowness  of  tone. 

2.  The  murmur  is  not  produced  at  the  tricuspid  orifice 
because  of  its  relationship  to  the  right  ventricular  first  sound; 
for  when  the  murmur  is  quite  well  marked  in  the  second  inter- 
space the  tricuspid  first  sound  can  as  a  rule  be  heard  to  be 
quite  pure  and  free  from  murmur  on  listening  over  the  sternal 
ends  of  the  fifth  and  sixth  interspaces. 

3.  The  ready  variability  of  the  mm-mur  shows  that  it  is 
not  due  to  any  permanent  damage,  but  suggests  that  it  is  due 
to  some  transient  cause — such  as  the  over-distension  of  some 
elastic  structm-e — that  can  readily  return  to  its  normal  size 
after  the  disturbing  factor  is  withdrawn  :  such,  indeed,  as  the 
over-distension  of  the  elastic  pulmonary  artery  and  the  readily 
dilatable  part  of  the  right  ventricle. 

4.  Its  point  of  maximal  intensity,  area  of  audition,  and 
direction  of  conduction  are  all  in  favour  of  its  pulmonary 
artery  origin. 

5.  Its  causation  must  be  closely  connected  with  the  up- 
ward dilation  of  the  right  ventricle,   because  within  certain 


264 


ANEMIA  OF  ADOLESCENCE 


well-defined  (and  easily  explainable)  limits  the  loudness  of 
the  murmur  is  proportional  to  the  amount  of  upward  increase 
of  the  cardiac  dullness  which  is  present. 

This  is  shown  by  the  following  table  giving  the  amount  of 
dilatation  present,  together  with  the  loudness  of  the  murmur, 
in  a  consecutive  series  of  over  200  cases  of  anaemic  heart  failure 
upon  which  274  observations  were  made. 

Increased  Loudness  of  the  murmur  accompanied  In- 
creased Upward  Dilatation  of  the  heart.— The  relationship 
which  the  loudness  of  the  pulmonary  artery  systolic  murmur 
bears  to  the  amount  of  upward  dilatation  of  the  right  ventricle 
is  well  shown  in  the  following  table,  which  gives  an  analysis 
of  274  observations  upon  204  cases  of  anaemia  which  showed 
upward  dilataion  of  the  heart,  and  a  pulmonary  systolic 
murmur  either  separately  or,  more  usually,  combined. 

In  this  table  very  loud  murmurs  are  those  heard  widely 
over  the  chest  and  well  conducted  into  the  vessels  of  the  neck. 


Loudness  of  the  Pulmonary  Artery  Systolic  Murmur  in  Relation 
TO  the  Upward  Dilatation  of  the  Right  Ventricle 


u 

,    u 

m 

. 

a 

4J 

h5 

' 

<73 

a 

s 

C    U 

a  a 

fl 

o 

j 

.Amount  of  dilatation  of  the  right  ventricle 

u 

a 

31 

+3 

c 

S  3 

73 

3 

§ 

n 

'  IS 

upwards  and  to  the  left 

a 

o 

1 

1 

'3 

^1 

3 

^1 
1 

&i 

'Slight' 

1 

6 

9 

8 

'  Present '           .          .          .          . 

2 

— 

2 

3 

4 

— 

11 

1     11 

'  Considerable "... 

— 

— 

— 

— 

— 

1 

1 

1 

J  inch  to  ^  inch  in  second  space 

2 

3 

6 

7 

5 

— 

23 

17 

f  inch  in  second  space 

3 

6 

5 

2 

8 

2 

26 

20 

1  inch           ,,           „           .          . 

4 

3 

8 

17 

16 

3 

51 

32 

1^  inch          , 

, 

1 

0 

6 

8 

8 

4 

27 

21 

li  inch          , 

, 

— 

— 

3 

11 

8 

7 

29 

23 

If  inch          , 

', 

— 

1 

2 

4 

8 

7 

2  inches         , 

. 

— 

— 

2 

6 

4 

19 

14 

More  than  2  inches  in  second  space 

— 

— 

— 

1 

1 

3 

3 

3  inches  or  more    ,,         ,,         ,, 

— 

— 

1 

— 

— 

2 

2 

None  in  second  but  2  in.  in  third 

1 

1 

3 

2 

— 

14 

10 

„  2A  „ 

1 

1 

2 

3 

— 

2 

9 

7 

„  3     „ 

— 

— 

— 

— 

— 

1 

1 

1 

None  in  second  but  some  in  third 

1 

— 

2 

1 

— 

— 

4 

3 

No  dilatation    .... 

10 

4 

10 

5 

3 

0 

32 

19 

No  notes  as  to  dilatation   . 

1 

— 

1 

3 

— 

— 

5 

5 

Total 

27 

19 

53 

83 

63 

29 

274 

204 

PULMONARY  SYSTOLIC  MURMUR 


265 


Loud  murmurs  are  those  conducted  up  to  the  clavicle  and 
outwards  along  the  first  part  of  the  subclavians.  Sometimes, 
however,  a  loud  murmur  may  be  fairly  localised.  Moderately 
loud,  faint,  and  very  faint,  murmurs  are  those  having  smaller 
areas  of  audition  and  the  less  degrees  of  loudness  which  their 
description  implies. 

In  this  table,  if  attention  be  confined  to  those  cases  which 
show  less  than  two  inches  of  relative  cardiac  dullness  in  the 
second  left  interspace,  it  is  evident  that  the  loudness  of  the 
murmur  increases  with  the  increase  in  the  amount  of  dullness. 
When,  however,  there  is  a  larger  amount  of  dullness  than  this, 
the  same  continuous  increase  in  the  average  loudness  of  the 
murmur  is  not  noticeable,  and  occasional  cases  are  met  with 
where  the  murmur  is  faint  or  even  absent. 

These  cases  will  be  explained  later,  and  in  the  meantime 
it  can  be  stated,  having  regard  to  the  above  statistics,  that 
for  moderate  amounts  of  dilatation  the  loudness  of  the  pul- 
monary systolic  murmur  is  proportional  to  the  amount  of 
upward  dilatation  of  the  right  ventricle  which  is  noticeable 
in  the  second  left  interspace. 

This  same  law  is  also  confirmed  by  the  few  cases  tabulated 
where  there  was  no  increase  of  dullness  in  the  second  inter- 
space, but  where  there  was  a  broadening  of  the  cardiac  dullness 
in  the  third  interspace.  The  following  summary  of  the  above 
table  shows  these  facts  rather  more  clearly  : — 

Loudness  of  Mtjemue 


Amount  of  dullness 

Obser-     Faint  and    !     i.r„;i„„<.„ 
vations     very  faint         Moderate 

Loud  and 
very  loud 

Loud 

Very 
loud 

Under    1    inch    in 
second  space 

1  inch   of   dullness 
in  second  space 

1}  inch  to   If  inch 
in  second  space 

2  inches  and  more 
in  second  space 

49     '22  =  40% 
51       11=22% 
64       10  =  15% 
24     ,  3  =  12i% 

9  =  18  % 
17  =  34% 
20  =  31  % 

9  =  37% 

15  =  30% 
19  =  38% 
33  =  51  % 
12  =  50% 

26% 
32% 
28% 
29% 

4% 

6% 

15% 

20% 

The  next  point  in  confirmation  of  the  theory  here  advanced 
as  to  the  causation  of  the  pulmonary  artery  murmur  is  that 
whenever  the  amount  of  cardiac  dullness  in  the  second   or 


266  ANiEMIA  OF  ADOLESCENCE 

third  interspace  shows  a  iem'porarij  increase  from  change  in 
the  attitude  of  the  patient  or  from  excited  action  of  the  heart, 
the  murram'  also  is  correspondingly  increased  in  loudness. 

The  increase  in  the  cardiac  dullness  which  results  from 
change  of  attitude  in  these  cases  of  upward  dilatation  of  the 
ventricle  is  usually  very  marked.  This  increase  of  the  cardiac 
dullness  is  probably  due  mainly  to  the  action  of  gravitation 
acting  in  two  ways  :  firstly,  by  causing  the  heart  to  assume 
a  somewhat  lower  position  in  the  erect  than  in  the  recumbent 
attitude,  as  is  shown  by  the  alteration  in  the  level  of  the  apex 
{vide  p.  312) ;  secondly,  the  heart  being  largely  fixed  by  the 
attachment  of  its  pulmonary  artery  and  aorta  to  the  roots  of 
the  lungs  (and  to  the  tissues  of  the  posterior  mediastinum),  the 
weight  of  the  heart  increases  to  a  certain  extent  the  tension 
of  the  anterior  wall  of  the  pulmonary  artery  and  the  adjacent 
part  of  the  anterior  wall  of  the  ventricle  when  the  patient  is 
standing,  and  this  tends  to  restrain  dilatation.  When  lying, 
this  tension  is  removed,  and  slightly  more  dilatation  takes  place 
therefore  in  that  position. 

The  following  are  some  notes  of  the  amount  of  this  increase 
of  the  cardiac  dullness  in  the  second  left  interspace  when  in 
the  recumbent  as  compared  with  the  erect  attitude. 

In  fourteen  cases  where  there  was  no  dullness  when  the 
patient  was  standing,  the  following  amounts  of  relative  dullness 
appeared  in  the  second  interspace  when  the  patient  lay  down  : 
I  inch  in  one  case  ;  f  inch  in  four  cases  ;  1  inch  in  five  cases  ; 
1|  inches  in  three  cases,  and  1|  inches  in  one  case.  In  ten 
other  cases,  where  there  was  some  dilatation  when  standing, 
there  was  an  increase  of  from  |  to  1|  inches.  In  two  of  these 
there  was  1  inch — namely,  from  \  inch  to  1|  inches,  and  from 
1  inch  to  2  inches ;  and  in  two  there  was  increase  of  1|  inches 

The  twenty-four  cases 

\  inch  on  lying  down. 
1 

2  J»  >> 

3 

4  J5  >> 

-■•  )>  5> 

11 

-•^4         5)  J> 

•'-2       "  " 


— namely,  from  1  inch  to  2|  inches. 

may  be  summed  up  as 

follows  : — 

Two  cases  showed 

an  increase  of 

One  case          „ 

Eight  cases      „ 

Seven     ,,         „ 

Three      „ 

Three      „ 

PULMONARY  SYSTOLIC  MURMUR  267 

The  fact  that  most  of  these  cases  show  large  amounts 
of  increase  of  dullness  is  due  to  the  fact  that  the  cases  seen  were 
hospital  out-patients,  and  the  greater  degi'ees  of  increase  were 
more  apt  to  be  noted  than  the  smaller  amounts  which  required 
more  careful  observation  for  their  detection. 

In  addition  to  these  twenty-four,  in  ten  other  cases  the 
fact  of  an  increase  in  the  amount  of  relative  dullness  in  the 
second  left  interspace  was  noted,  but  its  amount  was  not 
stated. 

These  cases  are  simply  illustrative  of  the  increase  of  dullness ; 
for  if  it  had  been  more  systematically  noted  it  would  have 
been  recorded  as  occurring  in  most  of  the  .patients  where 
upward  dilatation  of  the  right  ventricle  was  well  marked. 

A  similar  increase  of  the  cardiac  dullness  is  also  often 
noticeable  when  the  heart  begins  to  act  rather  more  excitably 
from  exertion  or  from  nervousness.  With  the  increase  of 
dullness  produced  in  either  of  these  ways,  there  is  almost 
invariably  an  increase  in  the  loudness  of  the  pulmonary  systolic 
murmur. 

The  following  facts  illustrate  this  point : — 

The  effect  of  change  of  position  upon  both  the  amount  of 
relative  dullness  in  the  second  left  interspace  and  the  pulmonary 
systolic  murmur  was  noted  in  twenty-seven,  instances,  and  in 
twenty-five  of  these  both  the  murmur  and  the  dullness  were 
increased.  Of  the  remaining  two  there  was  no  distinct  change 
in  one,  and  in  the  other  the  murmur  was  louder  in  the  erect 
attitude.     This  case  is  discussed  later  {vide  p.  303). 

This  increase  of  the  loudness  of  the  murmur  in  the  recum- 
bent attitude  is  so  characteristic  as  to  be  almost  diagnostic. 
The  effect  of  attitude  upon  the  murmur  was  also  definitely 
noted  in  twenty-eight  other  cases,  although  no  note  was  made 
as  to  the  presence  of  any  accompanying  increase  in  the  cardiac 
dullness.  Out  of  these  twenty-eight  cases  the  "mm-mm-  was 
definitely  increased  on  lying  down  in  twenty-four  cases.  In  two 
of  these  there  was  no  change,  and  in  two  the  murmur  was 
slightly  louder  when  the  patient  was  standing  up. 

Thus,  out  of  the  fifty-five  cases  noted,  the  murmur  was 
louder  in  the  recumbent,  attitude  in  forty-nine,  and  of  the 
remaining  six  there  was  no  change  in  its  loudness  in  three  ; 


268 


ANEMIA  OF  ADOLESCENCE 


and  in  the  other  three  it  was  louder  in  the  erect  than  in  the 
recumbent  attitude. 

Increased  Loudness  Due  to  Excited  Action  of  heart. 
—Increased  loudness  of  the  pulmonary  artery  murmur  is  also 
commonly  noticeable  under  conditions  somewhat  alUed  to 
those  just  mentioned— namely,  during  the  slight  increases 
in  the  heart's  activity  which  result  from  exertion  or  from 
nervous   excitement.    Such  increase  in  the  heart's   activity 

Cases  showing  an  Inconstant  and  Variable  Pulmonary  Mubmitr 


?<:l"ab3 

Apex 

ext  to 
V.N.L. 


Fig.  77. 

Maria  G.,  aged  twenty-one. 
Showing  size  o£  heart  during 
full  expiration.  Pulmonary 
murmur  sometimes  very  loud, 
sometimes  almost  absent. 


Fig.  78. 

Eliza  S.,  aged  twenty. 
Showing  amount  of  dilatation 
and  area  of  murmur  on  lying 
down  immediately  after  exer- 
tion.   None  when  erect. 


will  tend  to  increase  the  loudness  of  the  murmurs  in  two  ways 
— namely,  by  increasing  the  relaxation  of  the  artery  (owing  to 
the  increased  upward  dilatation  of  the  ventricle)  and  also 
by  temporarily  increasing  the  blood  pressure  in  the  pulmonary 
artery  whereby  the  over-distension  is  caused. 

Here  are  two  such  cases  taken  from  the  notes  of  my  out- 
patient cases. 

A  girl  of  eighteen  who  had  paid  two  fortnightly  visits  to  the 
hospital  and  was  rapidly  improving,  but  still  had  one  inch  of 
relative  dullness  in  the  second  left  interspace,  had  a  loud 
pulmonary  murmur  when  she  first  lay  down  on  the  couch  for 
examination,  but  it  rapidly  got  less  and,  in  the  course  of  two 
or  three  minutes,  almost  entirely  disappeared.  Also  in  a  young 
woman  aged  twenty-one,  who  had  a  very  considerable  amount 
of  right  ventricular  dilatation  {pide  fig.  77 :  the  murmm-  is 
noted  as  '  being  very  loud  at  times  [during  the  ten  or  fifteen 


PULMONARY  SYSTOLIC  MURMUR  269 

minutes  that  the  examination  of  the  heart  lasted]  and  at  times 
almost  inaudible.'  Slight  variations  in  the  exeitabihty  of  the 
heart's  action  being  sufficient  to  make  this  great  difference  in 
the  loudness  of  the  murmur  (see  also  fig.  78). 

Other  cUnical  features  which  tend  to  support  the  view 
here  advocated  as  to  the  pulmonary  murmur  being  due  to  an 
abnormal  distension  of  the  pulmonary  artery  are  the  frequent 
association  of  a  loud  pulmonary  second  sound  with  this  murmur 
and  also  the  fact  that  these  cases  do  not  as  a  rule  show  any 
signs  of  tricuspid  regurgitation,  for  leakage  through  the  tri- 
cuspid valve  would,  as  has  already  been  pointed  out,  tend  to 
prevent  the  intraventricular  pressure  from  risiiig  to  a  sufficient 
height  to  cause  upward  dilatation  of  the  ventricle  and  over- 
distension of  the  pulmonary  artery  in  these  cases. 

Where  this  type  of  dilatation  of  the  right  ventricle  in 
adplescents  is  secondary  to  severe  valvular  disease  of  the  left 
side  of  the  heart,  it  is,  however,  common  to  find  tricuspid 
regurgitation  and  dilatation  of  the  ventricle  to  the  right, 
associated  with  upward  dilatation  of  the  ventricle  and  a 
pulmonary  artery  murmur. 

Having  now  referred  to  the  clinical  facts  which  support 
the  main  thesis  here  advanced  that  the  basal  haemic  murmur 
of  anaemia  is  due  to  the  over-distension  of  the  pulmonary 
artery  which  is  brought  about  by  the  upward  dilatation  of 
the  right  ventricle,  we  must  now  go  rather  more  fully  into  the 
various  factors  concerned  in  order  to  prepare  the  way  for  the 
explanation  of  the  exceptions  to  the  rule  laid  down  which 
are  from  time  to  time  met  with. 

In  noting  the  presence  or  absence  of  a  pulmonary  artery 
murmm-  in  a  long  series  of  cases  showing  dilatation  of  the 
right  ventricle  upwards,  the  observer  camiot  fail  to  be  struck 
with  the  seeming  want  of  certamty  as  to  whether  any  particular 
type  of  case  will  have  a  loud  pulmonary  murmm-  or  not. 

For  instance,  I  have  stated  that  dilatation  of  the  right 
ventricle  upwards  so  as  to  cause  increased  dullness  in  the 
second  left  interspace  is  the  usual  cause  of  the  murmur,  and 
yet  in  some  of  the  cases  where  the  dilatation  is  extreme  no 
murmur  is  audible.     Again,  whereas  in  one  case  where  tlis 


270 


ANiEMIA  OF  ADOLESCENCE 


upward  dilatation  is  moderate  in  amount  the  murmur  is 
very  loud ;  in  another  apparently  similar  case  it  is  faint  or 
absent  (see  figs.  79  to  81).  And  again,  a  patient  who  is  very 
ill  and  breathless  may  have  a  faint  murmur,  and  yet  at  a 
subsequent  visit,  when  undoubtedly  better,  there  may  be  a 
loud  murmur  with  or  without  an  increase  instead  of  the 
lessening  in  the  amount  of  dilatation  which  her  improvement 
W'Ould  suggest. 

Moderate  Upward  Dilatation  of  Right  Ventricle,  but  no  Pulmonary 
Murmur.     (The   Cause    of   the   Absence    of   a   Murmur  was    not 

Investigated.) 


Fig.  79. 

Kate  L.,  aged  twenty-eight. 
Moderate  dilatation,  but  no 
pulmonary  mvirmur. 


Fig.  80. 

Sarah  S.,  aged  eighteen. 
Dyspnoea,  with  pulsation  and 
some  dullness  in  second  space, 
but  no  murmur. 


In  some  cases  the  murmur  is  present  where  there  is  no 
dilatation. 

Again,  although  the  murmur  is  as  a  rule,  greatly  increased 
when  the  patient  lies  down,  an  occasional  case  is  met  with 
where  this  is  not  the  case  and  the  murmur  may  even  be  louder 
when  the  patient  is  standing  up. 

These  exceptions  to  the  rule  do  not,  however,  shake  the 
evidence  which  has  been  adduced  as  to  the  cause  of  this  murmur, 
and  they  can  quite  easily  be  shown  to  be  confirmatory  of  it. 


Factors  Concerned  in  the  Production  of  the  Pulmonary 
Artery  Systolic  Murmur 

Several  factors  must  be  recognised  as  being  concerned 
in  the  production  of  the  pulmonary  systoKc  murmur,  and 
unless  their  relative  importance  is  recognised  it  will  not  be 


PULMONARY  SYSTOLIC  MURMUR 


271 


possible  to  understand  the  seeming  uncertainty  as  to  whether 
this  murmur  will  be  well  marked  or  not  in  any  particular  case 
of  dilatation  of  the  right  ventricle. 

1.  The  factor  of  prime  importance  is  the  over-distension 
of  the  first  part  of  the  pulmonary  artery,  whereby  instead 
of  being  cylindrical  it  becomes,  during  systole,  more  nearly 
globular,  resembling  an  aneurysm,  and  consequently  the  blood 
within  it  develops  eddies  and  the  aneurysmal  murmur  which 
they  cause. 

2.  Together  with  this  first  factor  must  be  noted  the 
alteration  in  the  direction  of  the 

axis  of  the  pulmonary  artery, 
as  compared  with  that  of  the 
ventricle,  which  tends  to  favour 
the  production  of  eddies  in  the 
dilated  artery. 

3.  The  third  main  factor  is 
the  relative  proportion  between 
the  size  of  the  pulmonary  orifice 
through  which  the  blood  enters 
as  compared  with  the  size  of  the 
dilated  pulmonary  artery  itself. 

For  the  production  of  eddies 
it  is  necessary  that  the  orifice  of 

entrance  be  smaller  than  the  vessel  into  which  the  blood 
is  entering.  If  the  orifice  of  the  pulmonary  artery  be 
normal  in  size  and  the  artery  beyond  be  abnormally  dis- 
tended during  systole,  the  production  of  eddies  and  the 
resulting  murmur  will  occm-. 

If,  however,  the  orifice  be  dilated  to  the  same  extent  as 
the  artery,  the  vessel  will  retain  its  normal  cylindrical  form, 
in  spite  of  its  dilatation,  and  no  murmm'  will  result. 

Of  these  three  factors  the  second  one  need  not  be  further 
discussed  as  there  is,  so  far  as  I  know,  no  evidence  that  variation 
in  the  loudness  of  the  murmur  is  ever  due  to  its  variation — 
if  such  were  possible. 

The  first  factor — namely,  the  distension  of  the  pulmonary 
artery — is  an  important  one,  and  must  be  analysed  into  its 
component  parts,  for  it  depends  upon  the  relationship  between 


Fig.  81. 


Kate     B., 


aged  nineteen.  Some 
dilatation  in  second  space  and  accentu- 
ation o£  pulmonary  second  sound,  but 
no  murmur.  A  tricuspid  systolic  and 
right  ventricle  third  sound  present. 


272  ANEMIA  OF  ADOLESCENCE^ 

the  internal  pressure  in  the  artery  and  the  resisting  power 
of  the  arterial  wall. 

Distension  of  the  artery  will  not  only  occur  with  a  normal 
or  slightly  raised  intra-arterial  pressure  in  conjunction  with  an 
arterial  wall  weakened  by  relaxation,  but  it  may  also  occur 
in  an  artery  with  walls  of  normal  tension  if  the  blood  pressure 
is  sufficiently  raised. 

Also  relaxation  of  the  wall  of  the  pulmonary  artery  will  not 
suffice  to  produce  a  murmm-  if  the  blood  pressure  be  so  lowered 
— as  a  result  of  myocardial  weakness — that  it  is  insufficient 
to  distend  the  relaxed  vessel  fully. 

Upon  the  possible  variations  in  the  relationships  of  these 
two  elements  in  the  causation  of  the  mm-mur  a  good  many 
of  the  exceptional  cases  depend. 

The  third  main  factor  also  is  variable  where  extreme  degrees 
of  dilatation  are  concerned,  for  it  is  almost  certain  that  the 
faintness  or  absence  of  a  puhnonary  murmur  which  is  noticeable 
in  extreme  cases  of  dilatation  is  due  to  the  fact  that  the  orifice 
of  the  pulmonary  artery  partakes  in  the  enlargement  of  the 
adjacent  part  of  the  right  ventricle. 

This  question  will  be  taken  up  rather  more  in  detail  later 
on,  and  in  the  meantime  this  factor  can  probably  be  left  out 
of  consideration  when  deahng  with  the  ordinary  cases  wdiich 
are  usually  met  mth. 

In  the  ordinary  cases  we  meet  with,  the  agencies  producing 
the  murmur  are  a  relaxation  of  the  elastic  wall  of  the  pul- 
monary artery  owning  to  its  origin  being  approximated  to  its 
termination  by  the  upward  dilatation  of  the  right  ventricle, 
combined  w^ith  a  blood  pressure  in  the  artery  of  normal  amount 
and  often  distinctly  in  excess  of  the  normal. 

Now  the  loudness  of  the  murmur  depends  upon  the  degree 
in  which  these  two  things  are  present. 

Given  a  constant  blood  pressure,  the  greater  the  relaxation 
the  greater  the  murmur ;  or  given  a  constant  degi'ee  of  relaxa- 
tion, the  greater  the  blood  pressure,  the  greater  the  murmur. 
The  ready  variabihty  of  the  murmur  can  be  understood  when 
it  is  remembered  that  increase  in  the  intraventricular  pressure 
increases  not  only  the  relaxation  of  the  artery  by  dilating  the 
ventricle,  but  also  increases  the  amount  of  the  distension  of 


PULMONARY  SYSTOLIC  MURMUR  273 

the  relaxed  artery,  and,  in  addition,  the  force  by  which  the 
murmur-producing  eddies  are  caused  in  the  dilated  artery. 

As,  however,  the  blood  pressure  does  not  as  a  rule  vary  very 
much  in  these  cases,  as  far  as  its  murmm'-producing  power  is 
concerned,  provided  that  temporary  variations  by  recent 
exertion  and  excitement  are  eliminated,  it  may  be  left  out  of 
consideration  m  the  majority  of  the  cases  met  with.  Therefore, 
when  dealing  with  an  ordinary  series  of  cases  it  can  be  asserted 
that  the  loudness  of  the  pulmonary  artery  murmm'  will 
depend  upon  the  degi-ee  of  relaxation  of  the  vessel,  and  this 
is  directly  proportional  to  the  degi'ee  in  which  the  level  of 
the  pulmonary  valves  are  raised  by  the  upw^ard  dilatation  of 
the  ventricle. 

This  statement  is  borne  out  by  the  table  at  p.  264,  when 
it  is  seen  that  the  average  loudness  of  the  murmur  gradually 
rises  as  the  amount  of  dilatation  increases  imtil  the  dilatation 
reaches  the  somewhat  extreme  amount  of  two  inches  or  so, 
when  variation  of  the  third  main  factor  begins  to  interfere 
with  the  loudness  of  the  murmur. 

What  has  just  been  said  ma}^  be  stated  in  the  following 
series  of  propositions  : — 

1.  When  the  arterial  w^all  is  relaxed,  as  above  described, 
the  murmm'  will  be  faint  or  absent  if  the  blood  pressure  be 
too  low  (owing  to  cardiac  weakness)  to  distend  the  artery 
adequately. 

In  such  a  case,  as  the  patient  gets  less  anaemic  and  less 
breathless,  it  may  sometimes  be  fomid  that  the  murmur  in- 
creases in  loudness  without  any  definite  change  in  the  amount 
of  dilatation  present,  owing  to  the  improvement  in  the  blood 
pressure. 

2.  When  the  blood  pressure  is  sufficient  to  distend  the 
artery  adequately,  the  loudness  of  the  murmur  will  be  dis- 
tinctly proportional  to  the  amount  of  relaxation  and  to  the 
height  of  the  blood  pressure  in  the  artery  in  each  particular 
case. 

3.  Apart  from  relaxation  of  the  arterial  wall  (such  as  we  are 
speaking  of),  it  is  possible  for  a  murmm-  to  be  produced  by 
over-distension  of  the  pulmonary  artery  provided  that  the 
right  ventricle  is  strong    enough   to   develop    and    resist   an 

T 


274  ANiEMTA  OF  ADOLESCENCE 

intraventricular  pressure  which  is  in  excess  of    the  resisting 
power  of  the  arterial  wall. 

4.  When  the  other  factors  are  constant,  the  loudness  of 
the  pulmonary  systolic  murmur  will  he  proportional  to  the 
smallness  of  the  pulmonary  orifice  in  comparison  with  the  size 
of  the  dilated  artery,  and  conversely  faintness  or  ahsence  of 
the  murmur  will  occur  when  the  pulmonary  orifice  is  so  dilated 
that  its  size  approaches  that  of  the  dilated  artery. 

I  believe  the  pulmonary  artery  murmur  in  such  a  case  as 
the  following,  where  (although  there  was  some  yielding  of  the 
anterior  wall  of  the  ventricle)  the  murmur  was  louder  in  the 
erect  than  in  the  recumbent  attitude,  was  due  mainly  to  the 
action  of  the  excessive  blood  pressure  upon  the  elastic  tissue 
of  the  arterial  wall,  and  was  therefore  louder  with  the  somewhat 
more  strongly  acting  heart  which  is  associated  with  the  erect 
posture. 

Case  showing  a  pulmonary  systolic  murmur  due  mainly 
to  excessive  blood  pressure  in  the  pulmonary  artery  : — 

The  patient  was  a  young  man  aged  twenty,  who  was  seen  in 
December  1891,  complaining  of  breathlessness,  which  prevented 
him  from  working.  There  was  no  history  of  rheumatism  or  other 
ailment,  and  the  exact  cause  and  mode  of  onset  of  his  heart 
trouble  was  not  noted.  On  examination,  the  heart  was  found 
to  be  acting  tumultuously,  and  was  often  irregular.  It  was 
found  to  be  dilated  upwards  and  to  the  left,  and  a  systolic 
pulmonary  murmur  was  present,  but  there  was  no  other  murmur 
to  be  heard. 

Two  days  later  the  heart  was  still  very  excitable,  and  there 
was  a  loud,  rough  systolic  murmur  heard  in  the  second  inter- 
space both  to  left  and  right  of  the  sternum,  and  the  pulmonary 
second  sound  was  very  much  accentuated.  There  was  no  mur- 
mur to  be  heard  at  the  apex,  but  the  first  sound  was  short  and 
sharp.  There  was  one  inch  of  relative  dullness  in  the  second 
left  interspace  with  well-marked  pulsation.  Both  the  pulmo- 
nary second  sound  and  the  pulmonary  murmur  were  fatinter 
when  he  was  lying  down  than  they  were  when  he  was  standing 
up.  A  month  later,  after  being  back  at  work  for  a  fortnight, 
the  murmur  was  not  audible  when  he  was  recumbent  and  the 


PULMONARY  SYSTOLIC  MURMUR  275 

heart  much  less  excitable.  The  patient  was  much  better, 
although  at  first  the  return  to  work  made  his  heart  bad  again. 
This  case  is  apparently  one  of  asthenia  of  a  transient  nature, 
mainly  involving  the  loft  side  of  the  heart — such  as  that  some- 
times due  to  influenza — and  the  right  ventricular  dilatation  was 
secondary  to  the  ineffective  action  of  the  left  ventricle  (vide 
p.  300). 

The  dilatation  of  the  conus  arteriosus  and  of  the  pulmonary 
artery  being  secondary  to  failure  of  the  left  ventricle  might  be 
expected  to  be  lessened  when  the  heart  was,  owing  to  the 
recumbent  attitude,  acting  more  quietly  than  when  the  patient 
was  erect. 

It  is  a  pity  that  in  this  case  no  definite  note  was  made  as 
to  the  effect  of  change  of  attitude  upon  the  cardiac  dilatation, 
for  there  is  httle  doubt  that  it  would  have  supported  the 
explanation  here  given  by  showing  no  increase  in  the 
recumbent  attitude. 

I  have  not  the  notes  available  of  any  similar  case  in  which 
a  pulmonary  murmur  existed  in  the  absence  of  an  upward 
dilatation  of  the  ventricle ;  but  such  are  not  very  infrequently 
met  with  in  somewhat  older  patients  than  those  here  dealt 
with,  and  more  especially  in  men. 

We  have  now  to  deal  more  fully  with  the  last  of  the  three 
main  factors,  and  to  point  out  its  importance  in  explaining 
some  of  the  cases  which  at  first  seem  atypical. 

As  already  stated,  it  is  essential  for  the  production  of  a 
murmur  in  the  dilated  artery  that  the  orifice  of  entrance  be 
smaller  than  the  internal  diameter  of  the  dilated  artery,  for 
if  the  pulmonary  orifice  be  dilated  equally  with  the  artery 
no  pulmonary  murmur  can  be  produced. 

This  is,  I  believe,  the  reason  why  in  most  of  the  extreme 
cases  of  this  type  of  dilatation  the  murmur  is  faint  and 
sometimes  entirely  absent. 

I  ought  to  be  able  to  furnish  pathological  proof  as  to  the 
size  of  the  pulmonary  orifice  in  these  cases ;  but  until  a  few 
months  ago,  they  were  to  my  mind  supposed  to  be  explicable 
by  a  much  more  doubtful  theory  which  I  have  held  (without 
due  analysis  as  is  too  apt  to  be  our  wont  in  matters  clinical) 
for  the  last  twenty  j^ears. 

t2 


276 


ANiEMTA  OF  ADOLESCENCE 


A  few  years'  observation  on  such  cases  might  give  some 
positive  evidence  on  this  point,  although  the  return  of  the 
structures  towards  normal,  after  death,  as  the  result  of  rigor 
mortis,  and  their  own  elasticity  would  have  to  be  reckoned  with. 

On  turning  to  the  table  on  p.  264,  it  is  noticeable  that  out  of 
two  observations  where  there  were  three  inches  or  more  of 
dullness  in  the  second  left  interspace,  in  one  there  was  a  faint 
pulmonary  murmur,  and  in  the  other  only  a  moderately  loud 

Great  Dilatation  of  Right  Ventricle.     Pulmonary  Murmur  Faint 


P.N.I. 


Fig.  82. 

Ellen  Gr.,  aged  eighteen. 
Very  considerable  dilatation,  but 
pulmonary  murmur  only  audible 
in  second  left  interspace. 


Fig.  83. 

Sarah  D.,  aged  twenty- two. 
Great  upward  dilatation,  but 
faint  pulmonary  murnmr. 


one.  In  these  cases  of  extreme  dilatation — especially  in  those 
where  the  pulmonary  valves  he  in  the  first  interspace,  or  under 
the  first  rib,  it  is  by  no  means  infrequent  to  find  no  murmur 
at  all.  Such  are  the  cases  illustrated  by  figs.  82  to  85,  and 
at  p.  314. 

It  is  possible  that  in  some  cases  of  dilatation  —  and 
especially  in  those  where  dilatation  is  extreme — there  may 
be  another  reason  for  the  pulmonary  murmur  being  less  loud 
than  might  be  expected  :  although  the  artery  be  relaxed,  the 
pulmonary  orifice  not  materially  enlarged  and  the  blood  pressure 
sufficiently  high.  For  in  some  such  cases  the  artery  may  be 
prevented  from  becoming  sufficiently  globular  to  cause  a  loud 
murmur  because  of  the  support  its  walls  are  receiving  from  the 
adjacent  structures.  For  instance,  until  recently,  I  supposed  the 
absence  of  murmur  which  I  have  more  than  once  noted  in  cases 
of  pneumonia  with  great  upward  dilatation  of  the  right  ventricle, 


PULMONARY  SYSTOLIC  MURMUR 


277 


might  be  explained  by  the  support  afforded  to  the  puhiionary 
artery  by  adjacent  consolidation  of  the  lung  {vide  p.  224).  I 
now,  however,  think  it  more  hkely  that  these  cases  are  exphc- 
able  by  the  more  recent  theory  of  dilatation  of  the  pulmonary 
orifice. 

Again,  in  severe  cases  with  a  not  too  high  blood  pressure,  it 
is  possible  that  the  support  afforded  by  the  adjacent  structures 
(the  aorta,  bronchi,  &c.)  may  be  sufficient  materially  to  lessen 
the  amount  of  dilatation  of  the  artery  and  so  moderate  the 
loudness   of  the  murmur   that   would    otherwise    occm-.     Li 


toKL. 


(Tir.L.is 
sternum) 


Fig.  84. 

Emma  B.,  aged  seventeen. 
Very  ^eat  upward  dilatation, 
but  faint  murmur. 


Fig.  85. 


Ada  T.,  aged  seventeen. 
Considerable  dyspnoea ;  mudd 
dilatation  ;  but  pulmonary,  tri- 
cuspid, and  mitral  miumurs  all 
faint  and  inconstant. 


cases  where  the  pulmonaiy  valves  lie  at  the  upper  border  of 
the  first  rib,  the  extreme  upward  increase  of  the  right  ventricle 
must  greatly  hmit  the  space  available  for  any  dilatation  of 
the  pulmonary  artery ;  and  it  is  possible  that  the  external 
support  thus  afforded  must  be  recognised  as  hindering  the 
dilatation  of  the  artery  upon  which  the  murmur  depends. 
Li  these  cases  the  anterior  aspect  of  the  pulmonary  valves 
is  often  at  least  an  inch  away  from  the  anterior  chest  wall, 
thus  being  displaced  backwards  as  well  as  upwards ;  and  the 
space  available  for  the  pulmonary  artery,  considering  the 
close  proximity  of  the  transverse  arch  of  the  aorta,  must  be 
very  small.  On  the  other  hand,  the  extreme  elasticity  of 
the  fibrous  tissues  in  adolescence  must  not  be  forgotten  and 
the  possibihty  of  there  being  sufficient  displacement  of  the 
aorta  to  allow  of  this  dilatation. 


Tricuspid  and  Pulmonary  Murmurs  both  Present 
(The  Area  of  Audition  of  the  Murmurs  is  shown  by  dotted  Shading) 


Fig.  86. 

Annie  B.,  aged  fifteen. 


Fig.  87. 
Emily  B.,  aged  nineteen. 


-  v-jT  ext 
toNL 


Adelina  J.,  aged  nineteen. 
Tricuspid  systolic  fainter  if 
erect.  Very  faint  pulmonary 
and  no  mitral  murmur. 


Fig.  89. 

Amy  H.,  aged  nineteen. 
Some  dyspncea  and  faintness  ; 
pulmonary  and  tricuspid 
murmurs  when  recumbent, 
none  wtien  erect. 


Superior  Vena  Cava  Murmur,  but  no 

Tricuspid  Systolic 

(See  also  fig.  58.) 


Fig.  90. 

Emily  N.,  aged  twenty- 
two.  Considerable  dyspnoea. 
Well-marked  pulmonary  and 
tricuspid  murmurs. 


Sup.  VenS.^ 
Ca,va  mur^ 


PuIV 


Fig.  91. 

Eliza  P.,  aged  twenty. 
Loud  pulmonary  murmur ;  some 
dropsy  of  ankles.  Tricuspid 
regiu-gitation,  with  superior 
vena  cava  murmur,  but  no 
tricuspid  sj'stollc. 


TRICUSPID  SYSTOLIC  MURMUR  279 

In  this  connection,  I  may  say  that  I  have  seen,  in  a 
case  of  sudden  collapse  of  the  left  lung  in  a  young  woman, 
the  heart  shift  from  its  normal  position  to  such  an  extent 
that  within  a  very  few  days  its  right  border  was  in  the  left 
nipple  line  and  the  left  border  in  the  mid-axillary  hne — a 
sudden  movement  to  the  left  of  some  2  or  2|  inches  in  extent 
{vide  p.  371). 

Such  a  case  as  this  seems  to  point  to  the  fact  that — in 
adolescence,  at  all  events — we  must  not  speak  with  too  great 
certainty  about  the  root  of  the  lung  as  a  *  fixed  point,'  owing 
its  fixation  to  the  spine  by  means  of  its  fibrous  tissue. 

Other  Auscultatory  Phenomena 

Having  now  discussed  the  main  phenomena  associated 
with  the  heart  failure  which  is  apt  to  accompany  anaemia 
in  adolescence,  it  will  be  necessary  to  say  a  few  words  about 
some  of  the  less  important  physical  signs,  and  also  to  give 
some  cases  illustrating  what  has  been  said  in  the  previous 
pages. 

'  Bruit  de  Diable.' — This  well-known  venous  murmur 
which  is  so  frequently  heard  in  the  neck  in  cases  of  anaemia 
is  discussed  m  Essay  VII,  where  a  reprint  is  given  of  the 
writer's  article  on  '  Dilatation  of  the  Eight  Ventricle,'  which 
appeared  in  the  Lancet  in  1894,  and  also  at  p.  15. 

Murmurs  due  to  Tricuspid  Eegurgitation 

Although  definite  dilatation  of  the  heart  to  the  right  is 
by  no  means  common  in  the  heart  failure  of  anaemia  in  ado- 
lescence (it  occurred  in  8-5  per  cent,  of  the  cases  investigated), 
some  signs  of  tricuspid  regurgitation  were  noticeable  somewhat 
more  frequently — namely,  in  about  23  per  cent,  of  the  178 
cases,  when  definite  notes  as  to  its  presence  or  absence  were 
made  {vide  pp.  238,  355). 

In  one-fourth  of  the  cases,  the  murmur  was  only  faint. 
The  accompanying  figures  (Nos.  86  to  90)  show  the  shape  of 
the  area  over  which  the  murmur  was  audible. 


280  ANiEMIA  OF  ADOLESCENCE 

A  tricuspid  regui-gitation  in  these  as  in  other  cases  may 
also  show  its  presence  by  means  of  either  a  superior  vena  cava 
murmur  or  a  venous  valve  murmur,  with  or  without  one  or 
both  of  the  other  murmurs. 

Fig.  91  shows  a  case  where  a  well-marked  superior  vena 
cava  murmur  was  unaccompanied  by  a  tricuspid  systolic 
murmur.  There  was  a  well-marked  pulmonary  murmur  as 
well.  Fig.  99  (p.  288)  shows  a  case  where  there  was  a  well- 
marked  systolic  murmur  locahsed  over  the  valves  at  the 
junction  of  the  right  internal  jugular  and  innominate  veins 
with  a  tricuspid  and  also  probably  a  superior  vena  cava 
murmur. 


Cases  of  Gbeat  Dilatation  Show^ing  a  Faint  or  Absent 
Tricuspid  Systolic  Murmur 

Attention  has  been  drawn  (p.  265)  to  the  fact  that  where 
there  is  an  extreme  amount  of  upward  dilatation  of  the  right 
ventricle,  the  pulmonary  murmm*,  instead  of  being  loud,  is, 
as  a  rule,  faint  or  absent. 

The  same  phenomenon  is  also  sometimes  noticeable  in  the 
case  of  the  mm-mur  produced  at  the  tricuspid  orifice,  and 
fig.  92  shows  a  case  where  great  dilatation  of  the  right 
ventricle  to  the  right  was  unaccompanied  by  a  well-marked 
tricuspid  murmur. 

As  the  tricuspid  systolic  murmur  is  more  often  present 
than  absent  in  cases  of  extreme  dilatation  of  the  ventricle 
to  the  right,  some  different  explanation  must  be  sought  from 
that  which  explains  the  absence  of  the  pulmonary  murmur 
under  sunilar  circumstances.  IMoreover,  it  must  be  remembered 
that  the  tricuspid  systohc  mm-mm-  is  very  often  absent  when 
there  is  only  a  moderate  amount  of  tricuspid  leakage.  There- 
fore, the  explanation  of  the  feebleness  of  the  murmm*  in  the 
cases  here  given  is  probably  the  same  as  that  of  the  absence 
of  tricuspid  murmur  hi  other  cases — ^whatever  that  explanation 
may  be.  In  comiection  with  these  cases  of  considerable 
dilatation  but  no  murmur,  it  may  be  of  interest  to  give  the 
following    case    of    very  considerable    dilatation  of    the  left 


DILATATION  OF  LEFT  VENTRICLE 


281 


ventricle,  in  which  no  mitral  murmur  was  audible.  It  is  hardly 
possible  that  in  such  cases  the  mitral  valve  still  remains 
competent ;  but  there  is  no  means  of  proving  that  it  is  a 
case  of  mitral  regurgitation  without  a  murmur  as  can  be  done 
when  such  a  condition  occurs  in  connection  with  the  right 
ventricle. 

The  patient  was  a  girl  aged  twenty-two,  suffering  fi-om 
a  moderate  amomit  of  anaemia  and  considerable  dyspncea. 
There  was  some  upward  dilatation  of  the  right  ventricle,  for 


Considerable  Ventricular  Dilatation,  but  no  Regurgitant  Murmur 


(Ant 

{axil¥ 

{Ime 


Fig.  92. 

Eliza  E.,  aged  nineteen. 
Extreme  dilatation  ;  pulmonarj- 
miurmnr  not  loud.  Slight  true 
pulsation  in  neck  veins,  but  no 
tricuspid  murmur. 


Fig.  93. 

Minnie  S.,  aged  twenty-two. 
Extreme  dilatation  of  left  ven- 
tricle, but  no  mitral  systolic 
murmur. 

Pulmonary  murmur  present. 


there  w^as  an  inch  or  so  of  relative  dullness  in  the  second  left 
interspace  with  well-marked  pulsation,  but  only  a  faint  murmur. 
The  apex  was  m  the  anterior  axillary  line  in  the  fifth  inter- 
space ;  the  impulse  was  heaving  and  forcible,  and  the  first 
sound  a  little  rough,  but  there  was  no  true  systolic  mm-mur. 
There  was  no  tricuspid  mmmm%  nor  was  there  any  excess  of 
right  ventricular  impulse  in  the  fourth  and  fifth  left  interspaces 
{vide  fig.  93  and  also  fig.  88). 

Arterial  Compression  Murmur.  —  This  is  a  systoUc 
mm-mm*  produced  at  the  spot  where  the  subclavian  artery 
crosses  the  first  rib  and  which  is  not  infrequently  heard  in 
cases  of  anaemia  in  adolescence.  It  is  discussed  in  Essay  IV, 
which  deals  with  the  diagnostic  difficulties  associated  with 
dilatation  of  the  right  ventricle  {vide  p.  22G). 


2S2  ANiEMIA  OF  ADOLESCENCE 

Eight  Ventricle  Third  Sound  and  Mid-diastolic 
Murmur 

These  two  physical  signs  which  are  by  no  means  uncommon 
in  right  ventricular  failure  in  ansemia  are  discussed  in  the 
essay  before  mentioned  (p.  340),  which  contains  a  summary  of 
the  phenomena  found  in  dilatation  of  the  right  ventricle. 

Both  the  sounds  here  referred  to  are  not  at  all  loud,  and 
they  differ  in  this  respect  from  the  corresponding  sounds  on 
the  left  side  of  the  heart  which  result  from  mitral  stenosis. 
They  are  best  heard  when  the  binaural  stethoscope  is  but 
lightly  pressed  against  the  chest  wall. 

The  theory  of  air  conduction  by  a  binaural  stethoscope  neces- 
sitates a  diaphragm  whereby  the  sound  vibrations  of  the  chest 
wall  are  transmitted  to  the  air  in  the  stethoscope  tube.  The 
chest-piece,  by  imprisoning  a  portion  of  the  skin,  constitutes 
such  a  diaphragm,  and  it  will,  I  think,  be  found  that  the  most 
useful  form  of  chest-piece  is  one  so  constructed  that  a  variation 
in  the  firmness  with  which  the  stethoscope  is  applied  causes  a 
decided  variation  in  the  degree  to  which  the  imprisoned  disk 
of  skin  is  stretched. 

In  the  case  of  the  diastolic  murmur  and  third  sound, 
audible  over  the  right  ventricle  in  anaemic  dilatation,  the  sound 
is  so  faint  that  a  minimal  amount  of  stretching  of  the  '  skin 
diaphragm  '  is  desirable. 

The  theory  of  the  production  of  these  sounds  at  the  tricuspid 
orifice  is  quite  simple  if  the  expansion  theory  of  the  mid- 
diastolic mitral  murmur,  as  discussed  at  p.  427,  be  accepted. 

In  the  case  of  such  hearts  as  these  we  are  now  describing, 
two  factors  are  at  work  hindering  the  complete  emptying  of 
the  auricle  into  the  ventricle  during  the  expansion  phrase  of 
the  cardiac  cycle. 

Firstly,  the  heart  muscle  is  apt  to  be  lacking  in  vigour 
owing  to  malnutrition  resulting  from  the  anaemia,  and  its  vigour 
of  suction  is  likely  to  suffer  in  consequence. 

Secondly,  there  is  a  tendency  to  auricular  dilatation  owmg 
to  the  cardiac  failure,  and  this  will  tend  to  ensure  the  prolonga- 
tion of  the  flow  of  blood  from  the  auricle  into  the  ventricle, 
upon  which  the  development  of  a  third  sound  and  mid-diastolic 
murmur  depends.      If  the  auricle  holds  more  than  its  usual 


THIRD  SOUND  AND  DIASTOLIC  MURMUR 


283 


amount,  the  probability  of  blood  passing  through  the  valve, 
after  the  onset  of  the  relaxation  phase,  is  increased. 

If  carefuly  looked  for,  one  or  other  of  these  signs  of  incomplete 
aspiration  by  the  ventricle  will  often  bo  found  in  the  cardiac 
failure  of  anaemia.  In  my  series  of  cases,  I  have  its  presence 
noted  only  some  nine  times  as  occurring  over  the  right  ventricle 
and  ton  thnes  over  the  left ;   but  then  I  have  only  noted  the 

Cases   Illusteating   the   Occurrence   of  a  Right  Ventricular  Third 
Sound  and  Mid-diastolic  Murmur 


mid-diobstoUc 
mur2n.ur 


mur? 


Fig.  94. 

Clara  B.,  aged  nineteen.  Sliow- 
ing  area  of  audition  of  riglit  ventricle 
third  sound  and  mid-diastolic  murmur. 


Fig.  95. 

Clara  B.,  aged  nineteen.  Shoeing  area 
of  audition  of  pulmonary  and  tricuspid 

systolic  murmui-s. 


absence  of  this  sign  about  the  same  number  of  times ;  and 
if  the  presence  of  a  third  sound  audible  over  the  riglit  ventricle 
were  carefully  looked  for,  it  would  be  found,  I  beheve,  in  quite 
a  considerable  proportion  of  the  cases  of  well-marked  anaemic 
dilatation  of  that  ventricle.  The  following  are  three  well- 
marked  cases.  In  two  of  them  a  well-marked  third  sound 
occurred  over  the  right  ventricle,  and  in  the  third  over  the 
left  ventricle.  As  the  cases  are  also  interesting  from  other 
points  of  view,  they  are  given  in  some  detail. 

Clara  B.,  aged  nineteen,  came  to  hospital  suffering  from 
marked  anaemia,  with  breathlessness,  weakness,  and  troublesome 


284  ANiEMIA  OF  ADOLESCENCE 

indigestion  with  emaciation.  The  heart  was  considerably  en- 
larged upwards  and  to  the  left,  there  being  relative  cardiac 
dullness  on  full  expiration  for  nearly  2  inches  in  the  second 
interspace  and  to  beyond .  the  nipple  line  in  the  third  (i.e. 
3  inches  from  the  sternal  edge). 

The  apex  was  in  the  fourth  space,  three  inches  from  the 
sternum.  There  was  a  loud,  but  decidedly  localised,  pulmo- 
nary systolic  murmur,  best  heard  over  an  area  about  two  inches 
in  diameter,  and  there  was  a  well-marked  reduplication  of  the 
second  sound.  There  was  also  a  tricuspid  systoUc  murmur 
audible  over,  and  just  to  the  left  of,  the  lower  half  of  the  sternum, 
and,  in  addition,  a  well-marked  tliird  sound  followed  by  a  '  mid- 
diastolic '  murmur  audible  over  the  whole  of  the  right  ventricle, 
as  shown  in  figs.  94  and  95. 

In  such  a  case  as  this  it  is  easy  to  map  out  on  the  chest  the 
exact  position  of  the  interventricular  septum  by  studying 
carefully  the  area  over  which  the  third  sound  or  mid-diastolic 
murmur  is  heard.  The  same  is  true  of  cases  where  the  third 
sound  arises  in  the  left  ventricle,  for  the  sound  is  as  a  rule  so 
feeble  that  the  presence  of  the  interventricular  septum  limits 
its  audibihty  to  the  ventricle  in  which  it  arises. 

In  this  patient  the  erect  attitude  caused  a  lessening  in 
the  size  of  the  cardiac  dullness  and  a  total  disappearance  of 
all  three  murmurs  and  the  third  somid. 

This  patient  rapidily  improved  under  treatment  without 
rest  in  bed,  and  in  five  weeks'  time  the  heart  had  become  normal 
in  every  respect. 

In  such  a  case  as  this  with  a  well-marked  true  reduplication 
of  the  second  sound,  it  is  easy  by  means  of  a  double  chest-piece 
to  the  stethoscope  (the  so-called  differential  stethoscope) 
to  demonstrate  the  presence  of  four  cardiac  sounds — a  first 
sound,  the  two  halves  of  the  second  sound,  and  the  third 
sound. 

The  second  case  is  that  of  Kate  S.,  aged  twenty-one,  who 
was  suffering  from  anaemia  and  dyspepsia  with  cardiac  failure, 
when  she  came  to  hospital. 

When  recumbent,  there  was  no  relative  dullness  in  the  second 
interspace,  but  a  faint  pulmonary  murmur — which  was  not  well 
conducted — was  audible.  There  were  2  inches  of  relative 
dullness  in  the  third  space  (as  against  the  normal  1|  inches), 
and  the  apex  was  under  the  fifth  rib  in  the  nipple  line.     The 


THIRD  SOUND  AND  DIASTOLIC  MURMUR 


285 


only  other  murmur  present  was  a  well-marked  mid-diastolic 
one,  heard  over  the  point  of  maximum  impulse  of  the  right 
ventricle,  which  was  situated  in  the  fourth  space  half-way  to  the 
nipple  line. 

This  was  preceded  by  a  well-marked  third  sound  audible 
in  this  situation,  and  which  was  occasionally  to  be  heard  over 
the  greater  part  of  the  right  ventricle.  The  mid-diastohc 
murmur  was  also  sometimes  heard  over  this  wide  area.  These 
areas  are  sho^ni  in 
fig.  9G. 


In  the  following 
case  there  was  a 
third  somid  of  left 
ventricular  origin, 
but  it  was  apparently 
functional  in  charac- 
ter and  produced  in 
the  same  way  as  the 
right  ventricular  one 
now  being  discussed. 
As  the  case  is  a  very 
characteristic  one  of 
anaemic  heart  failure 
it  will  be  dealt  with 
somewhat  fully. 

The  patient  was 
a  young  woman  of 


mrea,  of 
audition. 

Sometimes 
^Always 


Fig.  96. 

Kate  S.,  aged  twenty-one.  Showing  area  of  audition 
and  P.M.I,  of  right  ventricle  third  sound  and  tricuspid 
mid-diastolic  murmur. 


twenty-two,  who  came  as  out-patient  to  the  hospital  in  March 
1892,  suffering  from  angemia  and  so  much  breathlessness  that 
she  could  barely  manage  to  walk  up  a  single  flight  of  stairs 
without  stopping  to  rest. 

There  was  shght  true  pulsation  in  the  veins  of  the  neck  and 
a  very  loud  '  bruit  de  diable  '  which,  as  usual,  disappeared 
entirely  when  lying  down.  The  heart  was  considerably  en- 
larged, and  there  was  \\  inches  of  relative  dullness  \\-\i\\  pul- 
sation in  the  second  left  interspace,  and  in  the  third  and  fom-th 
spaces  the  dullness  and  pulsation  reached  to  the  nipple  line — 
i.e.,  3  inches  from  the  sternum.  The  apex  was  in  the  fifth 
space  in  the  nipple  line,  and  the  right  border  was  about  \  inch 
to  the  right  of  the  sternum. 

The  pulmonarj'  second  sound  was  greatly  accentuated,  and 


ANEMIA  OF  ADOLESCENCE 


the  shock  due  to  tlio  closure  of  its  valves  could  be  clearly  felt 
over  an  area  f  inch  in  diameter,  at  the  sternal  end  of  the  second 
left  interspace.  The  second  sound  was  distinctly  reduplicated, 
although  its  two  component  parts  were  not  completely  separated 
from  one  another.  The  area  over  which  the  double  sound  was 
audible  is  marked  in  fig.  97.  There  was  also  a  well-marked  third 
sound,  heard  best  over  a  small  area  1  inch  internal  to  the  apex  ; 
but  as  its  area  of  audition  extended  outwards  towards  the  apex. 


T^iid-dicLSt? 


Fig.  97. 

Alice  K.,  aged  tweaty-tvvo. 
Dilated  heart  and  areas  of  audition 
of  reduplicated  second  sound  and 
of  the  third  sound  and  mid-diastolic 
mitral  murmur. 


Fig.  98. 

Alice  K.,  aged  twenty-two.  Showing 
area  of  audition  of  systohc  murmur  at  base 
of  heart  (probably  a  pulmonary  tricuspid 
and  a  superior  vena  cava  murmur),  also  a 
mitral  svstolic. 


rather  than  inwards  towards  the  sternum,  its  point  of  origin 
was  almost  certainly  at  the  mitral  valve  rather  than  the 
tricuspid.  The  presence  of  a  faint  mitral  systolic  murmur, 
suggesting  some  dilatation  of  the  left  ventricle,  tended  to 
confirm  this  diagnosis.  The  third  sound  was  not  constantly 
present.  In  this  case  it  was  possible  with  a  differential  stetho- 
scope to  demonstrate  the  three  diastolic  sounds — namely,  the 
two  halves  of  the  second,  and  the  third  sound.  In  addition, 
there  was  a  systolic  murmur  audible  over  the  pulmonary  artery 
which  appeared  to  be  conducted  downwards  to  the  fifth  rib  and 
also  across  to  the  right  of  the  sternum,  and  especially  so  into  the 
second  right  interspace.  [This  last  named  must  have  been  a 
superior  vena  cava  murmur.] 


ILLUSTRATIVE  CASES  287 

Although  this  was  noted  as  only  one  murmur,  more  careful 
study  would — there  is  no  doubt — have  certainly  shown  that  the 
portion  below  about  the  third  rib  was  really  a  true  tricuspid 
murmur,  and  that  the  portion  to  the  right  of  the  sternum  in 
the  second  and  adjacent  interspaces  was  really  a  superior  vena 
cava  murmur.  Change  of  position,  holding  of  the  breath,  and 
the  effect  of  exertion  would,  by  varying  the  loudness  of  one 
or  other  portion,  have  sufficed  to  differentiate  the  three 
murmurs  the  one  from  the  other  {vide  fig.  98) . 

This  case  is  of  interest  as  confirming  what  has  been  said 
as  to  the  changes  due  to  consohdation  of  the  fibrous  tissues 
of  the  heart  wall  and  pericardium.  It  is  a  border-line  case 
between  the  adolescent  and  adult  types  of  dilatation.  In 
addition  to  well-marked  upward  dilatation  of  the  anterior 
wall  of  the  right  ventricle  there  was  some  general  yielding  as 
well,  as  was  sho"\\'n  by  the  dilatation  of  the  heart  to  the  right 
and  the  evidence  of  tricuspid  regurgitation  which  was  given 
by  the  tricuspid  murmur,  the  superior  vena  cava  murmur, 
and  the  presence  of  some  regurgitant  pulsation  in  the  veins 
of  the  neck.  Further,  the  presence  of  some  functional  mitral 
regurgitation  showed  that  the  right  ventricle  was  strong  enough 
to  allow  an  amount  of  exertion  capable  of  slightly  over-straining 
the  left  ventricle.  Had  the  right  ventricle  been  weaker — as 
would  have  been  the  case  earlier  in  life — the  girl  would  have  had 
to  give  in  sooner  and  would  not  have  been  able  to  continue  her 
work  until  she  overtaxed  her  left  ventricle  as  well  as  her  right. 

This  patient  also  rapidly  improved,  and  the  heart  is  noted 
as  being  nearly  normal  in  live  weeks'  time. 

Cases  Illustrating  Cardiac  Dilatation  in  the  Anaemia  of 
Adolescence 

It  will  now  be  well  to  emphasise  what  has  already  been 
said  as  to  the  character  of  the  dilatation  of  the  right  ventricle 
in  anaemia,  and  the  murmurs  which  accompany  that  dilatation, 
by  giving  a  series  of  cases  showing  the  outline  of  the  cardiac 
dullness  and  the  areas  over  which  the  various  murmurs  were 
audible.  Before  doing  so,  however,  it  is  necessary  to  say  a 
few  words  in  explanation  of  the  extreme  diversity  in  the  shape 


288 


ANEMIA  OF  ADOLESCENCE 


of  the  cardiac  dullness  in  tho  different  illustrations,  and  also 
of  the  apparent  want  of  correspondence  between  the  amount 
of  dilatation  and  the  loudness  of  the  murmur  or  the  area  over 
which  it  is  heard. 

The  reason  for  the  great  variability  of  the  physical  signs 
here  spoken  of  is  to  be  found  in  the  large  number  of  factors 
that  come  into  play  in  connection  with  the  production  of  the 
dilatation  and  of  the  murmurs. 

Case  of  An.idmia  showing  a  High  Apex  Beat  and  a  Normal  Diaphragm 


Tricuspids 
murmur  ' 
he&,rdJiere 


Apex,  if 
^T-ecumhent 
Apex  when 

erect 
FAint 

sr-st. 

TTiurF 


Fig.  90. 

Vivian  P.,  aged  seventeen.  Upward  dilatation ;  loud  pulmonary 
murmur,  tricuspid  murmur,  and  third  sound,  also  faint  mitral  systolic 
murmur. 

There  was  a  venous  valve  murmur  in  the  nook. 


It  might  be  wellj  therefore,  in  this  connection  to  summarise 
the  main  factors,  commencing  with  those  which  are  most 
important. 

The  prime  factors  in  causing  the  dilatation  are  the  increased 
resistance  in  the  pulmonary  artery  and  the  abiht}^  of  the 
muscles  of  the  right  ventricle  to  develop  sufficient  power  to 
overcome  it.  Both  these  are  extremely  variable,  depending 
on  the  degree  of  aniemia  and  the  degree  to  which  the  nutrition 
of  the  heart  muscle  suffers  from  the  antemia.  Upon  this 
last  factor  also  depends  the  power  which  the  right  ventricle 
has  of  resisting  the  tendencv  to  dilate,  which  is  the  natural 


ILLUSTRATIVE  CASES 


289 


consequence  of  the  increased  resistance  in  the  lungs.     Now 

the  adequate  filHng  of  the  left  ventricle  will  depend  upon 

the  success  which  the  right  ventricle  attains  in  its  effort  to 

pass  the  anaemic  blood  through  the  lungs,  and  there  is  every 

reason  to  beheve  that  the  apex  of  the  heart  is  more  displaced 

upwards  where  the  ventricle  is  badly  filled  than  when  it  is 

of  normal  size.      This, 

then,  is  a   factor  whicll    ''  <^ase  of  Anaemia  showing  a  High  Apex 

.  Beat  with  a  High  Diaphragm 

causes  a  most  stnkmg 

change  in  the  shape  of 

the  cardiac  area. 

Again,  a  similar 
change  to  this  last  will 
result  in  those  cases 
where  the  amount  of 
mahiutrition  or  the 
cardiac  weakness  is 
sufficient  to  cause  a  rise 
in  the  diaphragm  owing 
to  a  lessening  of  the 
total  volume  of  the 
blood  in  circulation. 

The  change  in  the 
outhne  of  the  cardiac 
dullness  which  results 
from  this  cause  is  well 
shown  in  the  first  two 
99  and  100. 


Fig.  100. 

Florence  P.,  aged  eighteen,  October  19,  1911. 
ilarked  dilatation  of  right  ventricle  upwards ;  high 
diaphragm,  and  moderate  pulmonary  murmur. 


cases   which  follow.     Compare   figs. 


Variations  in  the  Shape  of  the  Cardiac  Dullness 

The  shape  assumed  by  the  cardiac  dullness  in  this  type  of 
dilatation  is  well  show^i  by  the  figures  given ;  but  it  may  be 
well  to  say  a  word  or  two  as  to  the  frequency  of  the  various 
types. 

The  most  usual  is  where  there  is  a  moderate  amount  of 
outward  dilatation  proportional  to  the  amount  of  pm'e  upward 
increase,  thus  giving  the  heart's  dullness  an  evenly  rounded 
contour,  such  as  is  shown  in  figs.  00,  09,  94,  &c. 


290  ANAEMIA  OF  ADOLESCENCE 

Sometimes  there  is  only  upward  dilatation  present  and 
without  any  other  alteration  in  the  normal  shape  of  cardiac 
area  {vide  fig.  81). 

Occasionally,  a  well-marked  amount  of  upward  dilatation 
is  accompanied  by  a  good  deal  of  displacement  upwards  of 
the  apex,  but  without  any  dilatation  in  the  third  left  inter- 
space— thus  giving  an  irregular  outhne  to  the  cardiac  dullness, 
as  is  shown  in  figs.  101  and  103. 

In  this  instance  the  conus  arteriosus  alone  appears  to  be 
dilated.  In  such  cases  as  this,  it  is  apparently  muscular 
feebleness  which  explains  the  absence  of  any  increase  outwards 
in  the  third  space,  because  dilatation  is  apt  to  occur  here  also 
as  the  patient  improves. 

Another  type  which  is  sometimes  seen  is  one  characterised  by 
broadening  of  the  cardiac  dullness  in  the  third  left  interspace 
without  any  increase  upwards  {vide  fig.  107). 

The  statistics  as  to  age  in  relation  to  the  amount  of  dilatation 
shows  that  this  is  more  apt  to  occur  in  older  than  in  younger 
patients  {vide  following  table). 

Average  age  of  153  cases  of  anaemic  dilatation        .    19-3  years. 
73  cases  with  1  inch  or  less  of  dilatation  in   the 

second  interspace        .         .         .         .         .     19-4     „ 
46  cases  with  1|  to  1|  inches  of  dilatation  in  the 

second  interspace        .....     18'9     ,, 
15  cases  with  2  to  3  inches  or  more  of  dilatation  in 

the  second  interspace  ....     18'9    ,, 

20  cases  with  no  dullness  in  the  second  interspace, 

but  dilatation  in  the  third    ....     20-3    „ 

These  statistics,  therefore,  support  what  has  been  already 
said  (pp.  31,  33)  as  to  the  greater  tendency  to  upward  dilatation 
in  younger  patients. 

Two  Cases  of  Eaised  Apex  Beat  with  High  and  Normal 
Diaphragm  Eespectively 

The  following  are  two  ordinary  cases  of  anaemia,  showing 
an  ordinary  type  of  upward  dilatation  of  the  ventricle,  but  in 
the  one  case  the  diaphragm  was  high  and  m  the  other  normal. 


ILLUSTRATIVE  CASES  291 

Nevertheless,  in  both,  the  apex  of  the  heart  was  m  the 
fourth  interspace  when  the  patient  lay  down.  When  standing, 
however,  there  was  a  difference  :  for  the  low  diaphragm  of  the 
first  patient  allowed  the  apex  to  fall  mto  the  fifth  interspace 
when  in  the  erect  attitude  ;  the  high  diaphragm  of  the  second 
patient,  on  the  other  hand,  prevented  any  descent  of  the  apex. 

The  first  case  was  that  of  a  girl,  Vivian  P.,  aged  seventeen, 
who  was  suffering  from  anaemia  and  breathlessness.  There  was 
fullness  of  the  neck  veins  ;  a  loud  *  bruit  de  diable,'  also  false 
pulsation  and  some  true  pulsation  in  them.  There  was 
considerable  upward  dilatation  of  the  right  ventricle,  giving  1| 
inches  of  relative  dullness  on  ordinary  respiration,  with  pulsa- 
tion, in  the  second  interspace,  and  2  inches  in  the  third.  The 
apex  beat  was  in  the  fourth  interspace,  nearly  3  inches  from 
the  sternum,  but  dropped  into  the  fifth  interspace  when  the 
patient  stood  up.  There  was  a  little  absolute  dullness  in  the 
third  interspace.  There  was  no  increase  of  the  cardiac  area  to 
the  right.  The  Hver  was  normal  (as  shown  in  fig.  99),  both  as 
regards  the  right  and  the  left  lobes. 

Another  interesting  point  about  this  patient  was  that  in  spite 
of  her  age  being  only  seventeen,  there  was  well-marked  evidence 
of  tricuspid  regurgitation,  although  there  were  no  signs  of  any 
dilatation  of  the  right  ventricle  towards  the  right.  There  was 
a  faint  tricuspid  systolic  murmur  audible  over  the  area  shown. 
There  was  also  a  third  sound  of  right  ventricular  origin  audil')le 
over  the  area  marked  by  dark  dots  in  fig.  99. 

There  was  some  true  regurgitant  pulsation  in  the  neck,  and 
a  very  loud  systolic  murmur  and  palpable  thrill  observable  up 
to  the  angle  of  the  jaw.  In  addition,  there  was  the  false  pulsa- 
tion and  '  bruit  de  diable  '  usualh^  noticeable  in  anaemic  heart 
failure,  and  an  ordinary  pulmonary  systolic  murmur.  The 
systolic  thrill  and  murmur  in  the  neck  were  of  great  interest, 
for  they  were  not  observable  as  loudly  over  the  heart  or  in  the 
aortic  area.  Neither  were  they  to  be  found  along  the  hne  of  the 
subclavians,  as  is  the  case  with  an  arterial  compression  murmur 
{vide  p.  266). 

The  point  of  maximal  loudness  of  this  murmur — namely, 
just  above  the  clavicle — and  its  direction  of  conduction  up  to  the 
angle  of  the  jaw,  together  with  the  fact  that  it  was  not  loudly 
audible  also  in  the  subclavian  region,  made  it  certain  that  it 
must  be  produced  in  the  internal  jugular  vein. 

u  2 


292  ANEMIA  OF  ADOLESCENCE 

Tho  true  systolic  pulsation  in  the  neck  veins  showed  the 
presence  of  a  considerable  amount  of  tricuspid  regurgitation 
into  them,  and  the  cause  of  the  murmur  must  have  been  this 
blood  forcing  its  way  past  the  valves  which  guard  the  lower 
end  of  the  internal  jugular  vein  (;inde  p.  219). 

The  second  case  was  that  of  a  girl,  Florence  P.,  aged  eighteen, 
suffering  from  dyspeptic  symptoms  with  breathlessness  and 
only  a  moderate  amount  of  anaemia. 

The  chief  interest  in  connection  with  the  case  was  that  the 
lireathlessness  was  associated  with  a  high  diaphragm  on  the  left 
side,  and  the  suggestion  of  defective  circulation  which  this  sign 
afforded  was  confirmed  by  the  fact  that  the  pulmonary  murmur 
was  not  as  loud  as  might  be  expected  from  the  amount  of  cardiac 
dullness  and  pulsation  in  the  second  and  third  left  interspaces  ; 
for  in  the  latter  space  the  pulsation  could  be  felt  nearly  to  the 
anterior  axillary  line,  and  there  were  3|  inches  of  relative 
dullness.  There  was,  however,  a  loud  pulmonary  second  sound, 
and  the  right  ventricle  first  sound  was  louder  than  normal. 

The  apex  beat  was  in  the  fourth  interspace,  nearly  3| 
inches  from  the  sternum. 

There  was  some  reflex  disturbance  of  the  heart  and  circula- 
tion from  a  very  irritable  colon,  and  the  hands  were  apt  to  go 
blue  and  congested  and  the  heart's  action  was  at  times  too 
excited. 

Nevertheless,  the  case  shows  well  a  common  type  of 
ansemic  dilatation  of  the  right  ventricle  associated  w4th  a 
high  diaphragm  (fig.  100). 

Dilatation  mainly  involving  the  Conus  Arteriosus. — 
In  some  cases,  we  find  that  while  there  is  well-marked  dilatation 
of  the  heart  upwards  into  the  second  interspace  there  is  no 
lateral  broadening  of  the  cardiac  area  in  the  third  interspace. 
In  some  of  these  cases  the  outline  given  of  the  cardiac  area 
retains  more  or  less  its  normal  shape.  In  others,  although 
there  is  no  dilatation  in  the  third  interspace  there  is  in  the 
fourth,  often  accompanied  by — or  due  to — the  rise  of  the 
apex  of  the  heart  from  its  normal  situation  into  this  interspace. 
This  type  of  dilatation  gives  the  somewhat  striking  outline 
shown  in  the  figures  illustrating  the  following  cases. 

The  explanation  of  this  type  of  dilatation  must  be  found 
in  the  supposition  that  the  dilatation  only  involves  the  conus 


ILLUSTRATIVE  CASES 


293 


arteriosus  and  not  the  remainder  of  the  right  ventricle,  and  it 
is  confirmatory  of  the  modern  view  that  this  part  of  the  ventricle 
has  activities  and  functions  somewhat  mdependent  of  the  rest 
of  the  muscular  wall. 

Another  point  of  interest  which  is  brought  out  b.y  the  follow- 
ing clinical  histories  is  that,  where  this  type  of  dilatation  occurs, 

Case  of  An.^mia  Ilhtstrating  Dilatation  which   mainly  Involves  the 
CoNus  Arteriosus  of  the  Right  Ventricle 


ApexKl 


Fig.  101. 

Theresa  M.,  aged  twenty-three, 
March  12,  1891.  Showing  dilata- 
tion mainly  involving  the  conus 
arteriosus.  There  was  a  pulmonary 
nuirmur  and  a  slight  tricuspid. 


Fig.  102. 

Theresa  M.,  April  9, 1891.  Much 
stronger,  but  more  dilatation.  Pul- 
monary murmur  less  loud.  Increase 
of  cardiac  \  igour  had  caused  in- 
creased dilatation. 


it  is  sometimes  found  to  give  place  to  the  ordinary  type  of 
dilatation  as  the  patient  improves,  thus  suggesting  that  (owing 
to  muscular  feebleness)  the  increased  resistance  in  the  pulmonary 
artery  only  caused  dilatation  of  the  conus  arteriosus,  whereas  the 
return  of  a  good  measure  of  muscular  strength  caused  a  general 
dilatation  of  the  anterior  wall  of  the  usual  type.  A  more 
careful  study  of  such  cases  than  I  have  had  the  opportunity 
of  making  will  be  necessary  to  clear  up  the  theory  of  their 
origin  fully. 

The  first  case  is  that  of  Theresa  M.,  aged  twenty-three,  who 
came  to  hospital  March  12,  1891,  suffering  from  so  much 
dyspnoea  that  she  had  to  rest  two  or  three  times  on  going 


294 


ANEMIA  OF  ADOLESCENCE 


up  a  single  liight  of  stairs,  and  could  not  walk  a  mile  on 
the  level. 

There  was  but  little  anaemia  and  the  patient  was  well 
nourished.  The  heart  was  as  shown  in  figs.  101  and  102, 
and  in  the  following  table  of  measurements. 


Relative  cardaic  dullness 

March  12, 
1891 

April  9, 
1891 

April  30, 
1891              1 

To  left  of  sternum — 
2nd  space     . 
3rd     „          .          .          . 
4th     „          .          .          . 

5th     „         .          .          . 
To  right  of  sternum    . 

Inches 

1 

1 

(2^) 
3 

f 

Inches 

n 

2.1- 

3 

3 

Sternal  edge 

Inches 

0 

0 

3 

0 

There  was  a  moderately  loud  pulmonary  systohc  murmur 
on  lying  down,  also  audible  over  the  sternum  and  to  the  right 
of  it,  and  also  a  shght  tricuspid  murmur  and  some  false  but  no 
true  pulsation  in  the  neck  veins.  There  was  no  mm-mur  at 
the  apex.  A  month  later  when  she  was  much  better  and  able 
to  manage  one  flight  of  stairs  easily,  or  walk  five  miles  on  the 
level,  the  heart,  instead  of  being  smaller,  was  found  to  be  more 
dilated,  except  that  now  there  was  scarcely  any  relative  dullness 
to  the  right  of  the  sternum,  and  the  tricuspid  murmur  had  gone. 
In  spite  of  the  increased  amount  of  upward  dilatation  and  the 
increased  strength  of  the  heart,  the  pulmonary  murmur  was 
less  loud  and  was  now  not  at  all  well  marked.  Three  weeks 
later,  the  heart  had  returned  to  the  normal  size,  but  there  was 
still  a  slight  pulmonary  murmm-  to  be  heard  when  she  first  lay 
down,  and  there  was  still  some  dyspnoea  on  walking  uphill  or 
upstairs.  In  this  case  (as  in  the  next  one  to  be  referred  to) 
the  lessening  of  the  pulmonary  murmm*  must  have  been  due  to 
a  dilatation  of  the  orifice  of  the  pulmonary  artery  when  the 
increased  upward  dilatation  took  place. 

The  next  case  is  one  of  considerable  interest,  and  will  be 
therefore  dealt  with  rather  more  fully. 

The  following  case  is  of  interest  from  several  points  of  view  : 
Lizzie  G.,  aged  fifteen.  Seen  first  in  March  1891,  suffering 
from  anaemia,  palpitation,  and  dyspnoea  on  exertion  {vide 
fig.  103). 

On  examining  the  heart  it  was  found  to  show  the  less  usual 
type  of  upward  dilatation  of  the  right  ventricle,  which  suggests 


Case  showing  Dilatation  of  the  Right  Ventricle  which  mainly  Involves 
THE  CoNcs  Arteriosus 


Fig.  103. 

Lizzie  G.,  aged  fifteen,  March  7,  1891.  Dila- 
tation mainly  involving  the  conus  arteriosus. 
Very  loud  pulmonary  murmur.     Great  dyspncea. 


Fig.  104. 

Lizzie  G.,  April  4,  1891.  Very  much  better, 
but  more  dilatation,  and  pulmonary  murmur 
very  faint. 

Increased  cardiac  vigour  had  caused  increased 
dilatation. 


Fig.  105. 

Lizzie  G.,  May  2,  1891.  Improvement  has 
continued.  The  pulmonary  murmur  was  now  faint 
or  absent.    The  dilatation  had  lessened. 


Fig.  106. 

Lizzie  G.,  November  21,  1891.  Breathless 
and  ill  again.  Faint  pulmonary  murmur.  The 
original  type  of  dilatation  had  recurred. 


296 


ANiEMIA  OF  ADOLESCENCE 


that  the  dilatation  is  hmited  to  the  conus  arteriosus  and  does 
not  involve  the  rest  of  the  upper  part  of  the  ventricle  ;  for, 
although  there  was  one  inch  of  relative  cardiac  dullness  in  the 
second  interspace  there  was  only  the  normal  amount  in  the 
third  and  also  in  the  fourth  and  fifth.  There  was  a  very  loud 
pulmonary  systolic  murmur  audible  over  the  whole  of  the  upper 
part  of  the  chest  and  conducted  along  the  arteries  and  audible 
even  into  the  axillary  arteries.  There  was  no  tricuspid  murmur, 
and  although  there  was  a  murmur  at  the  apex,  the  possibility 
that  it  was  only  the  pulmonary  murmur  could  not  be  excluded. 
She  rapidly  improved,  and  at  her  third  visit  a  month  later 
stated  she  was  '  very  much  stronger,'  for  whereas  a  month  ago 
she  could  only  manage  to  walk  a  quarter  of  a  mile,  if  she  went 
very  quietly — and  even  then  w^ould  feel  tired  and  overdone ; 
she  could  now  walk  for  an  hour  easily.  Also,  whereas  a  flight 
of  stairs  caused  her  to  be  breathless  and  exhausted,  she  could 
now  do  a  flight  quite  easily  {vide  fig.  104). 

With  this  history,  it  might  be  expected  that  the  examination 
of  the  heart  would  show  that  it  had  returned  to  normal  and  that 
all  signs  of  dilatation  had  disappeared.  On  the  contrary, 
however,  examination  of  the  heart  demonstrated  the  fact  that 
it  was  decidedly  more  dilated  than  at  her  first  visit  (as  com- 
parison of  figs.  103  and  104  will  show),  except  in  so  far  as  the 
right  margin  of  the  relative  cardiac  dullness  was  concerned. 

The  accompanying  table  will  best  show  the  changes  that 
took  place  in  this  patient's  heart. 

Amount  of  Relative  Cardiac  Dullness  in  the  Several  Interspaces 


March  7, 

April  4, 

Mav2, 

Nov.  21, 

Dec.  19, 

Jan.  30, 

1891 

1891 

1891 

1891 

1891 

1892 

Inches 

Inches 

Inches 

Inches 

Inches 

Inches 

To  left  of 

sternum — 

2nd  interspace 

1 

u 

0(1) 

u 

1 

0 

3rd 

u 

2i 

n 

n 

u 

H 

4th 

H 

3^ 

3 

H 

31 

2 

5th 

H 

H 

4i 

4 

H 

^ 

To  right  of 

i 

Sternal 

0 

— 

— 

sternum 

edge 

1 

Pulmonary 

Very 

Very 

Faint  or 

Faint 

None 

None 

mtirmur 

loud 

faint  or 
absent 

absent 

General  condition 

Very 

Much 

Much 

Breath- 

Much 

Very 

breath- 

better 

better 

less 

better 

well 

less 

again 

ILLUSTRATIVE  CASES  297 

These  two  cases  illustrate  fairly  well  this  special  type  of 
dilatation  which  is  by  no  means  a  common  one  in  anaemia. 

It  is  remarkable  that  so  great  an  increase  in  the  dilatation 
of  the  right  ventricle  upwards  should  have  been  accompanied 
by  so  great  an  improvement  in  the  patient's  condition,  and  it 
strongly  suggests  the  conclusion  that,  at  first,  the  heart  muscle 
was  too  weak  to  develop  enough  intraventricular  pressure  to 
cause  dilatation,  and  that  (as  is  the  case  in  acute  myocardial 
damage)  dilatation  of  the  heart  was  here  a  sign  of  returning 
strength. 

The  outlines  of  the  cardiac  area  seem  to  show  that  this  patient 
was  always  apt  to  have  dilatation  of  the  conus  arteriosus  out  of 
proportion  to  the  adjacent  part  of  the  ventricle.  Another  point 
of  interest  here  is  the  lessening  of  the  pulmonary  murmur 
in  spite  of  increasing  upward  dilatation  and  increasing  strength. 
This  W'as  due  in  all  probability  to  dilatation  of  the  pulmonary 
orifice,  as  previously  suggested.  The  fact  that  in  this  case 
a  loud  pulmonary  murmur  was  never  again  noticeable  is  also 
in  favour  of  this  explanation.  When  seen  on  April  4,  there 
was  a  slight  tricuspid  systohc  murmur  audible  only  over  the 
right  ventricle. 

When  examined,  subsequently,  on  May  2  {vide  fig.  105), 
there  was,  as  is  so  often  the  case,  well-marked  reduphcation  of 
the  second  sound,  and  a  note  was  made  that  the  first  portion 
was  clearly  of  pulmonary  origin  and  the  second  half  of  aortic, 
and  that  the  pulmonary  half  was  (as  is  usual)  not  audible  at 
the  apex.  This  observation  can  with  care  be  often  made 
in  these  cases  of  anaemia,  thus  confirming  the  fact  that  in- 
creased pressure  in  the  pulmonary  artery  is  the  cause  of  the 
reduplication. 

Another  point  of  interest  in  this  case  is  that  she  suffered 
for  a  time  from  optic  neuritis  as  a  result  of  her  anaemia,  and 
Dr.  Lloyd  Owen  reported  in  May  the  presence  of  '  double 
optic  neuritis  with  a  medium  amount  of  exudation  and  great 
vascularity.' 

After  some  months,  she  came  under  treatment  again  for  a 
shght  return  of  her  anaemia  and  of  her  dyspnoea  ;  for  although 
she  could  now  walk  a  mile  with  fair  ease,  one  flight  of  stairs 
would  make  her  breathless.     She  had  also  some  dyspepsia, 


298 


AN.EMIA  OF  ADOLESCENCE 


which  probably  had  much  to  do  with  her  relapse.  Fig.  106 
and  the  above  table  show  that  the  same  typo  of  dilatation 
occurred  again,  and  they  indicate  the  changes  that  took  place 
in  the  heart  until  January  30,  1892,  when  it  was  quite  normal 
and  the  patient  quite  well  again. 

Dilatation  mainly  to  the  Left.— It  is  not  infrequent  in 
cases  of  anaemia  to  find  that  the  amount  of  dilatation  outwards 
in  the  third  and  fourth  left  interspaces  is  in  excess  of  that  in 
an  upward  direction.  Sometimes  the  whole  of  the  dilatation 
is  outwards  ;  and  if,  at  the  same  time,  the  lower  border  of  the 
heart  is  raised,  the  cardiac  dullness  loses  its  ordinary  shape 
and  is  very  wide  in  proportion  to  its  vertical  diameter. 

The  following  is  the  most  extreme  case  of  the  kind  of  which 
I  have  records  : — 

Mary  J.  R.,  aged  fifteen,  but  tall  for  her  age,  came  to  the 
hospital  on  November  14,  1891,  complaining  of  shortness  of 
breath,  palpitation,  and  indigestion. 

On  examining  the  heart  it  was  found  that  in  the  erect 
attitude  there  was  no  dilatation  upwards  or  to  the  right,  but  that 
there  was  cardiac  dullness  and  pulsation  for  4  inches  (i.e. 
nearly  to  the  anterior  axillary  line)  in  both  the  third  and  the 
fourth  left  interspaces.  The  lower  border  of  the  heart  was  at 
the  fifth  rib. 

On  first  lying  down,  |  inch  only  of  relative  dullness 
appeared  in  the  second  interspace,  but  after  a  few  minutes  this 
increased  till  there  was  1|  inches.  On  once  again  standing  up, 
the  dullness  was  slow  in  disappearing  again. 

The  size  of  the  heart  at  this  visit  and  one  paid  a  week  later 
is  best  shown  in  the  following  table : — 


November  14,  1891 

NOVEMBER  21,  1891 

Inter- 
space 

Erect 

Eecumbent 

Erect                       Recumbent 

Dullness 

Pulsa- 
tion 

Dullness 

Pulsa- 
tion 

Dullness 

Pulsa- 
tion 

Dullness 

Pulsa- 
tion 

Rela- 
tive 

Abso- 
lute 

Rela- 
tive 

Abso- 
lute 

Rela-  '  Abso- 
tive    1   lute 

Rela- 
tive 

Abso- 
lute 

2nd 
3rd 

4th 
5th 

Inches 
0 
4 
4 

Inches 
0 
0 
3 

Inches 

0  1  H 

+      ** 

famt     5 

i 
1 

Inches 
0 

Yes 
Yes 
Yes 
0  care 

Inches 
3 

H 

iac  du 

Inches 
0 
1 

llness 

or  pub 

Inches 

H 

4 
4 
ation. 

Inches 
0 

i 

+ 

1 

ILLUSTRATIVE  CASES 


299 


The  nipple  line  was  3  inches  from  the  sternal  edge  and  the 
anterior  axillary  Hne  was  4|  inches  from  it. 

The  pecuhar  shape  assumed  by  the  cardiac  dullness  is  shown 
in  fig.  107. 

When  erect  there  was  only  faint  pulsation  in  the  fourth 
interspace,  so  the  apex  beat  appeared  to  be  in  the  third. 

As  regards  the  heart  sounds  there  was  a  well-marked  pul- 
monary systohc  murmur  heard  over  the  second  and  third 


Two  Cases  of  An^jua  showing  Broadening  of  the  Cardiac  Area 


Fig.  107. 


ilary  J.  E.,  aged  fifteen,  Novem- 
ber 11, 1891.  Extreme  broadening  of 
the  cardiac  dullness.  Well  marked 
pulmonary  murmur. 


Fig.  108. 


Alice    G.,  aged  sixteen.      Great 

dyspncea.      Broad  cardiac   dullness 

with      pulmonary  and      tricuspid 
murmur. 


interspaces  and  conducted  towards  the  neck,  where  it  was  lost 
in  a  loud  mm'mur  of  subclavian  origin.  The  pulmonary  second 
sound  was  greatly  accentuated  and  there  was  a  '  bruit  de  diable  ' 
in  the  neck.  At  the  second  visit  the  pulmonary  mm-mur 
was  less  loud,  and  there  was  occasionally  a  faint  tricuspid 
murmur  to  be  heard  at  the  sternal  end  of  the  fom'th  left 
interspace. 

Also  at  this  visit  there  was  a  trace  of  relative  dullness  to 
the  right  of  the  sternum. 

Fig.  108  shows  another  case  where  there  was  almost  no  dull- 
ness in  the  second  interspace,  but  in  the  fourth  it  was  |  inch 
external  to  the  nipple  hne.  In  this  case,  too,  there  was  a  sUght 
tricuspid  murmur. 


300  ANEMIA  OF  ADOLESCENCE  ' 

Cases  Showing  no  Increased  Loudness  of  the  Pulmonary 
Systolic  Murmur  in  the  Kecumbent  Attitude 

We  must  now  speak  of  four  cases  where  the  puhiionary 
systolic  murmur  was  not  increased  when  the  patient  lay  down, 
and  SCO  if  it  is  possible  to  find  a  reasonable  explanation  why  these 
do  not  conform  to  the  general  rule,  for  the  test  of  a  theory  is 
its  ability  to  explam  the  exceptions  as  well  as  the  ordinary  cases. 

The  first  case  is  really  not  one  of  ansemia,  but  it  is  given 
here  as  an  instance  of  a  type  of  exception  to  the  rule  that  we 
may  occasionally  expect  to  meet  with.  It  has  been  referred 
to  at  p.  274. 

The  patient,  who  came  to  see  me  in  December  1891,  was  a 
man  aged  twenty,  suffering  from  breathlessness  with  occasional 
irregularity,  and  tumultuous  action  of  the  heart.  There  was  no 
history  of  rheumatism,  no  mitral  or  aortic  murmurs,  and  the 
main  abnormality  was  dilatation  of  the  right  ventricle  upwards 
and  to  the  left,  giving  one  inch  of  relative  dullness  and  also 
pulsation  in  the  second  left  interspace.  There  was  also  a  well- 
marked  pulmonary  systolic  murmur,  which  was  noted  as  being 
loud  and  rough  in  character.  There  was  great  accentuation 
of  the  pulmonary  second  sound,  and  it  was  well  heard 
in  the  second  interspace  to  the  right  and  the  left  of  the 
sternum. 

The  interesting  point  was  that  the  pulmonary  systolic 
murmur,  although  quite  loud  and  rough  when  he  was  standing, 
was  quite  faint  or  even  absent  when  he  lay  down.  It  was  also 
noticeable  that  the  pulmonary  second  sound  was  less  loud 
in  the  recumbent  than  in  the  erect  attitude. 

These  facts  give  the  key  to  the  solution  of  the  case.  It  is 
evident  from  the  rouglmess  of  the  murmur  and  the  loudness  of 
the  pulmonary  second  sound  that  the  wall  of  the  right  ventricle, 
although  slightly  dilated  upwards,  was  strong  enough  to  main- 
tain a  much  higher  mtraventricular  pressure  than  normal : 
the  need  for  this  higher  pressure  being  found  in  failure  of  the 
left  ventricle  from  influenza  or  other  cause,  and  as  to  the  nature 
of  which  I  have  no  record.  It  appears,  therefore,  that  the 
right  ventricle  in  this  case  was  sufficiently  strong  to  cause 
an  aneurysmal  dilatation  of  the  pulmonary  artery,  in  which 


ILLUSTRATIVE  CASES  301 

the  factor  of  intra-arterial  pressure  played  a  far  larger  part 
than  usual,  and  relaxation  of  the  arterial  wall  a  far  smaller 
part.     There  was  here  no  anaemia  to  cause  muscular  feebleness. 

Now,  as  the  murmur-producing   dilatation  seems  in  this 
case  mainly  due  to  the  abnormally  high  blood  pressure  it  is 
natural  for  the  murmur  to  become  less  with  the  quieting  of 
the  cardiac  action,  which  takes  place  on  lying  down.     In  this 
case  the  physiological  fact  that  the  heart  beats  more  quietly 
when  the  patient  lies  down  is  confirmed  by  the  lessening  in 
the  loudness  of  the  pulmonary  second  sound,  which  was  observ- 
able m  this  case  when  he  assumed  that  attitude.     We  may 
from  this  case  safely  make  the  following  generahsation  :    The 
increase  in  the  loudness  of  the  pulmonary  systolic  murmur, 
which  is  usually  observable  when  the  patient  lies  dowii,  must 
not  be  expected  in  those   cases  where  increase  in  the  intra- 
arterial pressure  plays  a  more  important  part  in  the  production 
of  the  aneurysm-like  dilatation  than  that  which  is  played  by 
relaxation  of  the  arterial  wall.     Each  of  the  four  exceptional 
cases  here  being  dealt  with  may  well  be  explained  by  this  same 
generalisation,  although  the  records  which  I  have  are  hardly  full 
enough  for  a  very  confident  statement.     The  cases  were  only 
hospital  out-patients,  and  were  seen  twenty-one  years  ago.     In 
one  of  them  the  patient  was  a  woman  of  twenty-seven,  in 
whom  the  ventricle  walls  would  presumably  be  stronger  and 
able  to  develop  a  higher  blood  pressure  than  in  the  majority 
of  the  cases  dealt  with  in  this  essay.     There  was,  moreover, 
a  tricuspid  systolic  murmur  present  as  well  as  the  pulmonary 
one,  thus  showing  that  the  thin  part  of  the  anterior  wall  of 
the  ventricle   ivas  losing   some   of  its    adolescent  weakness, 
and  that  the  chamber  was  more  inclined  to  dilate  as  a  whole 
than  simply  upwards  and  to  the  left. 

This  same  fact  was  also  suggested  by  there  being  no  increase 
of  cardiac  dullness  in  the  second  left  interspace,  although 
there  was  some  in  the  third  space — namely,  nearly  to  the  nipple 
line. 

The  systolic  pulmonary  murmur  was  faint,  but  was  not 
increased  on  lying  down,  neither  was  the  tricuspid  murmur 
louder. 

Presumably,  in  the  case  of  the  tricuspid  murmur  also,  the 


302 


ANiEMIA  OF  ADOLESCENCE 


Case  of  AKiEMiA  showing  no  Increase 
IN  THE  Loudness  of  the  Pulmonary 
Murmur  in  the  Recumbent  Attitude 


Pair 


lessening  in  the  cardiac  force,  duo  to  the  recumbent  position, 
fully  neutralised  the  increased  facility  for  regurgitation  up 
into  the  superior  vena  cava,  which  would  result  from  the 
absence  of  the  force  of  gravitation  {vide  fig.  109). 

Of  the  next  case  I  have  very  few  notes,  but  it  is  evidently 
one  of  the  same  nature  as  the  last  two.  There  was  only 
about  \  inch  of  relative  dullness  in  the  second  space,  and  it 
was  nearly  normal  in  the  third,  and  the  apex  was  low  in  the 

fourth    space     in     the 
nipple  line. 

There  was  a  pul- 
monary systolic  mur- 
mur localised  to  an 
area  some  two  inches 
in  diameter,  and  wliich 
was  louder  in  the  erect 
than  in  the  recumbent 
attitude.  The  patient, 
a  girl  of  nineteen,  was 
ansemic,  languid,  and 
breathless  {vide,  figs. 
110  and  111). 

The  .last  case — 
though  probably  of  the 
same  nature  as  the 
other  three — is  not 
quite  so  clear,  because 
a  mitral  murmur,  which 
was  present,  was  louder  in  the  recumbent  attitude.  Unfortu- 
nately, I  have  no  note  of  the  loudness  of  the  pulmonary 
second  sound  ;  but  the  fact  that  there  was  no  increase  in  the 
amount  of  the  upward  dilatation  of  the  right  ventricle,  w^hen 
lying  down,  is  in  favom-  of  the  theory  we  are  now  advocating. 
In  this  case,  too,  there  was  only  \  inch  of  relative  dullness  in 
the  second  interspace,  but  the  aj^ex  was  in  the  fourth  space 
I  inch  external  to  the  nipple  line. 

In  the  absence  of  fuller  notes,  a  certain  element  of  doubt 
must  attach  to  this  case.  It  is  also  possible  that  the  addi- 
tional loudness  in  the  erect  attitude  mav  have  been  due  to 


Fig.  109. 

Alice  A.,  aged  twenty-seven.      Pulmonary  murmur 
not  louder  if  recumbent. 


ILLUSTRATIVE  CASES 


303 


an  increase  in  the  loudness  of  the  superior  vena  cava  murmur 
rather  than  of  the  pulmonary  systolic. 

The  following  case  is  of  interest  as  confirming  what  has 
previously  been  said  with  regard  to  heart  failure  without 
enlargement  being  due  to  a  higher  degree  of  muscular  weakness 
than  is  the  case  when  enlargement  is  present. 


Case  showing  a  Pulmonary  Systolic  Murmtjr  Louder  in  the  Erect  than 
THE  Recumbent  Attitude 


Fig.  110. 

Edith  E.,  aged  nineteen.  Showing 
cardiac  area  and  area  of  murmurs  when 
erect.  The  murmur  on  the  right  may- 
be a  superior  vena  cava  murmur. 


Fig.  111. 

Edith  E.  Area  of  murmurs  when 
recumbent.  Pulmonary  systoUc  less 
loud.  Lessening  of  tricuspid  miu'mur 
also. 


In  this  case,  however,  the  dilatation  which  occurred  as 
soon  as  the  heart  began  to  get  stronger  may  have  been  partly 
due  to  the  fact  that,  owing  to  the  patient  not  being  confined 
to  bed  and  not  being  under  constant  medical  supervision,  she 
overstrained  her  heart  by  too  much  exertion. 

Had  the  patient  been  kept  quieter  it  is  probable  that  the 
dilatation  would  have  been  less  ;  but,  even  if  this  were  so, 
the  case  illustrates  very  well  the  diagnostic  value  of  dilatation 
as  pointing  to  good  muscular  strength  as  compared  with  the 
absence  of  dilatation  which  characterised  the  earlier  stages 
of  the  patient's  illness  when  there  was  evidently  considerable 
muscular  feebleness. 


304 


ANAEMIA  OF  ADOLESCENCE 


The  case  is  as  follows  : — 

Gertrude  L.,  aged  twenty-one,  a  watchchain-maker,  came 
to  the  hospital  September  15,  1891,  complaining  of  frequent 
fainting  attacks  and  great  dyspnoea.  She  was  very  anaemic, 
and  suffered  from  menorrhagia.  The  examination  of  the  heart 
showed  that  there  was  some  dilatation  upwards  and  but  httle 
to  the  left  and  none  to  the  right,  as  shown  in  fig.  112  and  in 
the. table,  p.  306. 

The  apex  was  in  the  fourth  interspace  in  the  nipple  Ime 

A  Case  of  An^.mia  showing  Increased  Loudness  of  the  Pulmonary 
Murmur  due  to  Increased  Cardiac  Vigour 


PulY 
murr 


Fig.  112. 

Gertrude  L.,  aged  twenty- 
one,  September  15, 1891.  Paint- 
ness  and  great  dyspnoea. 


Fig.  113. 

Gertrude  L.,  October  24. 
No  upward  dilatation.  Pul- 
monary murmur  louder.  Much 
better. 


when  the  patient  lay  down,  and  under  the  lower  border  of  the 
fifth  rib  when  she  was  standing  up.  I  have  no  doubt  that  had  I 
known  twenty  years  ago  the  importance  of  noting  the  level  of 
the  gastric  resonance  and  the  size  of  the  Hver,  I  should  in  this 
case  have  found  that  the  former  could  be  detected  in  the  fifth 
interspace,  and  that  the  absolute  dullness  of  the  liver  was  greatly 
reduced  in  size  :  pointing  to  a  degree  of  weakness  of  the  cardiac 
muscle  which  would  readily  account  for  the  feelings  of  faintness 
occurring  several  times  a  day — which  was  one  of  the  chief 
symptoms  of  which  she  complained. 

At  this  time  (September  15)  there  was  a  distinct  pulmonary 
murmur  localised  to  an  area  a  couple  of  inches  or  so  in  diameter 
with  its  centre  over  the  situation  of  the  pulmonary  valves.  She 
improved  under  treatment,  and  on  October  24,  was  decidedly 
better,  although  she  still  had  occasional  attacks  of  fainting.  Her 
palpitation   was  much   less,  and  she  could  now  go  up   two 


ILLUSTRATIVE  CASES 


305 


flights  of  stairs  without  having  to  stop,  whereas  she  could 
not  manage  a  single  flight  without  considerable  dyspnoea 
before  September  15. 


Extreme  Dil.vtatiox  axd  Absence  of  Pulmonary  Murmur 


Fig.  114. 

Gertrude  L.,  December  5, 
1891.  Very  greatly  improved, 
but  heart  greatly  dilated; 
pulmonary  murmur  not  loud. 


(V.Nl.^2%) 


Fig.  115. 

Gertrude    L.,    January 
1892.     Very   much   better. 


This  improvement  was  associated  with  a  slightly  lessened 
upward  dilatation  of  the  right  ventricle,  for  there  was  now  no 
dullness  in  the  second  left  interspace  as  against  an  inch  or  more 
which  was  noticeable  at  the  first  visit  {xiide  fig.  113). 

The  increased  muscular  power  of  the  heart  was  shown 
not  only  by  a  lessening  in  the  amount  of  upward  dilatation, 
but  also  by  an  increase  in  the  loudness  of  the  pulmonary 
murmur  :  showing  that  in  this  case  the  lessened  relaxation 
of  the  pulmonary  artery  was  more  than  counterbalanced 
by  the  increase  in  the  distensile  force  which  resulted  from  the 
improvement  in  the  tone  of  the  heart  muscle.  The  increased 
cardiac  strength  was  also  accompanied  by  a  lowering  of 
the  apex  beat  from  the  fourth  to  the  fifth  interspace,  due 
presumably  to  a  lowering  of  the  diaphragm. 

When  next  seen  on  December  5,  there  was  a  great  improve- 
ment in  the  patient's  condition ;  she  could  now  easily  go  up 
two  or  three  flights  of  stairs  and  walk  well,  and  had  httle 
breathlessness  except  when  suffering  from  nervous  excitement. 

Coupled  with  this  great  improvement  it  was  remarkable 
to  find  what  might  be  considered  a  great  deterioration  in 
the  condition  of  the  heart,  for  it  M'-as  very  greatly  dilated,  as 


306 


ANiEMIA  OF  ADOLESCENCE 


will  be  seen  by  a  glance  at  lig.  114  or  at  the  accompanying 
table. 

When  she  lay  clown,  the  relative  cardiac  dullness  reached 
up  to  the  first  rib  and  extended  out  to  beyond  the  nipple 
line  in  the  second  interspace  and  to  the  anterior  axillary 
line  in  the  third.  There  was  also  one  inch  of  relative  dullness 
to  the  right  of  the  sternum  in  the  third  and  fourth  interspaces, 
and    there  was  well-marked   cardiac    pulsation  all  over  this 


Interspace 

September  15, 1891 

October  24, 1891 

December  5,  1891 

January  2, 1893 

Erect 

Recum- 
bent 

Erect 

Recum- 
bent 

Erect 

Recum- 
bent 

^'^^"^         bent 

Inches 

Inches 

Inches 

Inches 

Inches 

Inches 

Inches       Inches 

2nd 

(U) 

— ■ 

2i 

3 

1 

3rd 

(2) 

(If) 

U 

4f 

1      2i 

4th 

21 

n 

3i 

3* 

1     3^ 

5th 

2| 

— 

2i 

— 

— 

— 

To  right 

Mid-st 

ernum 

Mid-st 

ernum 

—             1 

Right   edge 

of  sternum 

1               1 

Murmur 

Faint      Well 
marked 

Loud 

Not 
loud 

None 

Faint 

General 

Breat  hless 

Dysp  noea 

Dyspnoea 

condition 

and  faint 

much     less. 

much  less. 

Still  fa  int  at 

Genera  1    im- 

times 

1 

prove  ment 

1 

i 

area.  In  spite  of  the  great  upward  dilatation  now  present, 
the  pulmonary  systolic  murmur  was  not  at  all  loud. 

This  case  illustrates  very  well  the  interaction  of  the 
three  main  factors  to  which  the  pulmonary  systolic  murmur 
is  due. 

At  the  first  visit  there  was  relaxation  of  the  pulmonary 
artery  with  a  normal  pulmonary  orifice ;  but  the  murmur  was 
faint  because  the  ventricle  was  too  weak  to  supply  distensile 
force  enough  to  cause  an  aneurysmal  dilatation.  At  the 
second  visit,  with  lessened  relaxation  of  the  arterial  wall,  there 
was  nevertheless  a  loud  murmur  because  the  distensile  force 
was  great. 

At  the  third  visit  there  was  very  great  shortening  of  the 
artery  and  therefore  great  relaxation  of  its  elastic  wall,  com- 


ILLUSTRATIVE  CASES  307 

binecl  with  a  very  strongly  acting  ventricle — conditioas  certain 
to  produce  great  dilatation  of  the  artery ;  but,  nevertheless, 
the  murmur  was  faint  because  the  dilatation  was  presumably 
great  enough  to  involve  the  pulmonary  orifice  and  so  to  prevent 
the  production  of  eddies  in  the  dilated  artery. 

At  her  fourth  visit,  three  weeks  later,  the  cardiac  dilatation 
had  greatly  lessened  and  the  patient  was  much  stronger 
{vide  fig.  115). 


Essay  VL— THE  HEAET  IN  OVEESTEAIN 

Under  this  heading  those  cases  of  heart  failure  will  be 
dealt  with  where  excessive  physical  exertion  is  the  primary- 
factor  in  the  cardiac  failure  in  contradistinction  to  many  of 
the  cases,  already  dealt  with,  where  disease  played  a  more 
or  less  important  part  in  the  breakdown  of  the  circulatory 
apparatus. 

As  this  is  a  very  simple  cause  of  cardiac  failure,  the  giving 
of  a  few  cases  will  help  to  illustrate  the  part  which  simple 
overstrain  plays  in  cases  of  a  more  complicated  nature,  such 
as  those  due  to  anaemia  which  have  already  been  dealt  with. 
Looking  at  the  cases  of  overstrain  here  given,  it  will  be  evident 
that  as  a  rule  there  is  nothing  special  about  the  changes  in  the 
heart  which  are  fomid  in  them,  but  that  they  conform  very 
closely  to  the  changes  in  the  right  and  left  ventricles  already 
described  under  Heart  Failure  with  Enlargement  in  Adolescence 
in  Adult,  and  in  Later  Life,  and  also  in  the  essay  on  the 
Condition  of  the  Heart  in  Anaemia. 

It  has  just  been  said  that  this  question  of  the  effect  of 
ordinary  physical  overstrain  upon  the  heart  is  a  simple  one 
in  comparison  with  many  of  the  problems  which  face  us  in 
heart  failure  ;  but  even  here  we  are  met  at  the  outset  with 
a  question  wdiich  has  to  be  answered — namely,  '  When  the 
heart  is  overtaxed  by  physical  exertion,  does  the  pulmonary 
or  the  systemic  circulation  suffer  more  from  the  overstrain, 
or  are  both  equally  overtaxed  ?  '  In  endeavouring  to  answer 
this  question,  we  must  remember  w^hat  has  already  been  said 
as  to  the  difference  between  the  heart  of  the  adolescent  and 
that  of  the  adult — namely,  that  in  the  adolescent  the  heart's 
power  of  resisting  dilatation  depends  upon  its  muscular  wall, 
whereas  in  adult  life  the  fibrous  tissue  of  the  pericardium  and 
of  the  heart  plays  the  most  important  part,  and  that,  there- 

308 


THE  HEART  IN  OVERSTRAIN  309 

fore,  in  early  life  the  thinner  portions  of  the  heart  walls  are 
apt  to  dilate  before  the  thicker  parts,  whereas  later  in  life  this 
factor  does  not  play  anything  hke  so  important  a  part. 

If  this  fact  were  not  recognised,  we  might  make  a  mistake 
in  answering  the  question  we  are  at  present  considering, 
and  say  that  in  adolescence  and  early  adult  life  it  is  evident 
that  overstrain  affects  the  pulmonary  circulation  much  more 
than  the  systemic,  for  it  is  the  right  ventricle  alone  that  shows 
overaction  and  dilatation  in  early  life,  whereas  in  adult  and  later 
life  the  left  ventricle  appears  to  be  affected  by  overstrain 
to  about  the  same  extent  as  the  right,  or  possibly  more. 

This  statement  would  be  an  incorrect  answer  to  the  question 
now  considered.  We  know  that  the  ease  with  which  the  thin 
muscular  wall  of  the  right  ventricle  dilates  in  early  life  protects 
the  stronger  left  side  from  dilatation,  and  therefore  it  is  very 
difficult  to  tell  by  studying  such  cases  whether  the  burden 
of  overstrain  falls  mostly  on  the  systemic  or  the  pulmonary 
circulation.  In  adult  life,  when  we  have  reason  to  believe 
that  the  distensibility  of  the  two  sides  of  the  heart  is  much 
more  nearly  equal,  we  find  that,  in  overstrain,  the  two  sides 
of  the  heart  are  much  more  likely  to  be  equally  affected.  This 
is  not  a  point  to  which  the  Mi'iter  has  given  special  attention, 
and  therefore  all  that  can  be  said  here  is  that  there  does  not 
appear  to  be  any  great  disparity  between  the  extra  strain 
thrown  upon  the  right  heart  owing  to  the  call  for  more  rapid 
oxidation  of  the  blood,  and  that  thrown  upon  the  left 
owing  to  the  increased  arterial  supply  demanded  by  the 
muscles.  Doubtless  a  careful  comparison  of  a  series  of  cases 
would  show  that  overstrain,  due  to  exertion  which  necessitated 
fixation  of  the  chest  muscles — such  as  lifting  heavy  weights 
or  rowing — would  throw  more  strain  on  the  right  ventricle 
than  on  the  left,  whereas  rapid  general  movements  of  the  body 
. — such  as  those  required  for  bicycling — might  involve  the  left 
side  more  than  the  right.  Bicycle  racing,  where  fixation 
of  the  arms  and  chest  muscles  is  necessary,  would  probably 
come  under  the  former  category. 

The  well-knowTi  fact  that  in  athletes  it  is  the  breathing 
that  fails  first — as  shown  by  the  retracted  Ups  and  wide  open 
nostrils — must  again  not  be  taken  as  evidence  that  running,  &c.. 


310  THE  HEART  IN  OVERSTRAIN 

throws  more  strain  on  the  lungs  than  on  the  systemic  circula 
tion,  because  athletics  are  mostly  practised  by  young  men, 
in  whom  the  distensibihty  of  the  right  ventricle  protects  the 
left  from  overstrain,  and,  therefore,  even  though  the  strain  be 
wholly  on  the  systemic  circulation,  the  only  symptom  of  an 
overtaxed  left  ventricle  in  such  a  heart  will  be  embarrassment 
of  the  right  ventricle.  This  would  l)e  an  interesting  subject 
for  further  study. 

Before  giving  the  series  of  illustrative  cases  it  will  be  well 
to  say  a  few  words  as  to  the  meaning  of  the  term  '  overstrain.' 
The  actual  meaning  of  the  term  implies  that  a  heart  is  taxed 
beyond  its  powers  of  resistance  and  suffers  in  consequence — 
but  this  meaning  would  include  all  forms  of  heart  failure  ;  for 
a  weak  heart  can  be  as  much  overtaxed  in  carrying  on  the 
normal  circulation  as  a  normally  strong  heart  would  be  in  doing 
an  amount  of  work  in  excess  of  the  normal.  For  the  sake  of 
convenience,  however,  it  is,  I  think,  usual  to  limit  the  meaning 
of  the  term  to  what  may  be  called  absolute  (as  distinct  from 
relative)  overstrain — namely,  where  a  heart  with  no  evident 
signs  of  weakness  fails  through  being  overtaxed  by  an  excess 
of  work.  In  some  of  the  cases  here  given  there  was  some 
heart  weakness  present,  but  this  will  not  detract  from  the 
value  of  the  series  as  showing  the  type  of  heart  failure  fomid 
in  overstrain — as  apart  from  valvular  disease,  &c.  In  other 
words,  I  have  illustrated  this  subject  with  cases  of  relative 
overstrain  as  well  as  with  those  of  absolute  overstrain. 

The  first  few  cases  given  will  be  those  in  yornig  individuals, 
and  it  will  be  seen  that  the  type  of  dilatation  of  the  heart  is 
practically  the  same  as  that  described  in  the  essay  on  Anaemia. 
The  first  case  I  shall  give  is  an  ordinary  one  of  simple  dilatation 
of  the  right  ventricle  in  an  otherwise  quite  healthy  young  man, 
who  had  somewhat  overexerted  himself.  It  is  a  type  of  case 
very  frequently  met  with. 

J.  E.  B.,  a  young  man  aged  twenty-one,  with  no  anaemia 
and  of  thoroughly  healthy  appearance,  came  to  me  in  Jiily  1893, 
complaining  of  breathlessness  and  feeling  his  heart  lieat  too 
much  after  exertion.  There  was  a  history  of  overstrain  at  the 
age  of  fifteen,  when  he  felt  very  ill  and  weak  after  a  very  long 
hill-climb  on  a  bicycle.     Latterly,  he  has  only  had  dyspnoea 


THE  HEART  IN  OVERSTEATN 


311 


after  excessive  exercise — such  as  rowing  in  a  I'aco.  A  montli 
ago,  he  was  nearly  unconscious  for  the  last  half-mile  of  a  boat- 
race,  and  also  for  half  an  hour  afterwards. 

When  the  heart  was  examined,  it  was  found  to  be  actinf^ 
excitedly,  and  the  first  sound  was  too  forcible.  There  was  an 
abnormal  amount  of  pulsation  in  the  third  and  second  left  inter- 
spaces, but  only  when  in  the  recumbent  attitude,  and  in  the 
epigastrium  only  when  erect.  The  radial  pulse  was  fairly 
good,  but  there  was  some 
false  venous  pulsation  in  the 
neck,  and  the  veins  were  too 
full.  The  cardiac  apex  was 
in  the  fifth  interspace  in  the 
nipple  line.  Percussion  gave 
the  following  results  :  In  the 
erect  attitude  there  was  onlv 


Upward  Dilatation  of  the  Heart 
IX  Overstrain 


1|  inches  of  relative  cardiac 


Fig.  116. 

James  E.  B.,  aged  twenty-one.  fpwaril 
dilatation  of  right  ventricle  from  overstrain. 
Dilatation  increased  on  recumbency  without 
alteration  of  the  apex. 


dullness  in  the  third  left  inter- 
space— i.e.  a  normal  amount — 
but  on  lying  down  the  cardiac 
dullness  increased  markedly 
upwards,  and  the  relative  dull- 
ness was  found  to  extend  in 
the  third  interspace  to  the 
nipple — i.e.  2|  inches  and 
Ij  inches  of  relative  dullness 
appeared  in  the  second  left 
interspace.  The  position  of 
the  apex  did  not  change  at 
all,  so  this  increase  was  not 
due  to  a  mere  upward  displacement  of  the  heart  as  a  whole, 
as  is  sometimes  the  case.  In  the  erect  attitude  the  first  sound 
in  the  pulmonary  area  was  not  quite  pure,  but  there  was  not  a 
distinct  murmur.  When  lying,  however,  a  very  well-marked 
murmur  appeared  over  the  pulmonary  artery,  and  was  audil)le 
upwards  as  far  as  the  clavicles  and  episternal  notch  and  down- 
wards nearly  to  the  apex.  It  was  not  conducted  into  the  vessels 
of  the  neck,  nor  was  it  heard  loudly  enough  over  the  lower  part 
of  the  cardiac  area  to  suggest  the  presence  of  a  tricuspid  murmur 
as  well  as  a  pulmonary  murmur.  There  was  no  evidence  of 
dilatation  of  the  right  ventricle  to  the  right  {vide  fig.  IIG). 

Here,  then,  was  a  fairly  characteristic  case  of  a  right  ventricle 


WAen 
recumbent 
When 
erect 


312 


THE  HEART  IN  OVERSTRAIN 


which  had  given  way  as  a  rosiilt  of  simple  overstrain  in  a  healthy- 
young  man.  It  is  proba])lo  that  the  condition  of  the  heart 
was  not  altogether  the  result  of  the  recent  boat-racing  strain, 
but  that  the  bicycling  strain,  five  years  previously,  had  left  the 
heart  unduly  dilatable.  This  patient  was  examined  again  two 
years  later,  and  although  he  considered  himself  quite  well 
there  was  still  a  marked  pulmonary  murmur  present,  although 
there  was  almost  no  upward  dilatation  of  the  right  ventricle. 
There  was  also  a  well-marked  tricuspid  murmur  heard  over  the 


Area  if  recumbent 
-Aj-ea.  if  erect 

P.Kl  of  impulse 
when  recumbent 
"    erect 
rea  ±£ 
erect 


EiG.  117. 

Jeffrey  P.,  aged  fourteen.     Upward  dilatation  of  the  right  ventricle  from 
overstrain  of  a  weak  heart.     Showing  change  due  to  recumbency. 


right  ventricle  in  the  fourth  and  fifth  left  interspaces  and  faintly 
to  the  right  of  the  sternum. 

The  following  is  a  good  instance  of  the  results  of  simple 
overstrain  without  anaemia  in  a  boy  of  fourteen  (ri(?e  fig.  117) : — 

He  was  a  well-developed  and  well-nourished  lad — as  shown 
b}^  his  height  being  5  feet  \\  inches,  and  his  weight 
7  stone  10^  pounds — but  he  had  had  an  attack  of  rheuma- 
tism seven  months  previously,  and  had  slight  rheumatic 
pains  occasionally  since.  There  was  no  history  of  over- 
exertion, and  the  boy  had  not  been  to  school  since  his  ill- 
ness ;  l)ut  no  doubt  the  cardiac  dilatation  dated  from  shortly 
after  his  attack  of  rheumatism,  as  he  was  only  kept  in  bed 
three  weeks,  although  in  it  all  his  joints  were  involved  and 


THE  HEART  IN  OVERSTRAIN  313 

the  temperature  reached  102°  F.  on  one  or  two  occasions. 
The  cause  of  the  cardiac  failure  here  was  doubtless  the  soft- 
ening and  weakening  effect  of  the  rheumatic  poison  upon 
the  heart,  coupled  with  the  undue  strain  caused  by  the  l3oy 
being  allowed  to  get  up  too  soon,  before  the  heart  muscle 
had  recovered  from  the  effects  of  the  rheumatic  toxin.  The 
case  is,  therefore,  one  of  relative,  not  absolute,  overstrain.  The 
condition  of  the  heart  was  as  follows  :  There  was  about 
I  inch  of  relative  dullness  in  the  second  interspace,  and  a  well- 
marked  pulmonary  murmur  heard  there  when  the  patient  was 
Ij'ing  do'^Ti,  but  when  he  sat  up  there  was  no  dullness  in  the 
second  interspace  and  no  murmur.  To  the  right,  relative  dull- 
ness was  observable  just  to  the  right  of  the  sternum  in  either 
attitude.  There  was  some  sternal  dullness  to  the  level  of  the 
third  rib  when  recumbent,  and  to  a  less  extent  when  erect. 
The  apex  was  in  the  fourth  interspace,  just  external  to  the  nipple 
line  (3  inches  from  the  sternum)  when  recumbent.  When 
erect,  it  dropped  a  little  and  could  be  felt  in  the  fifth  interspace, 
and  some  pulsation  appeared  at  the  same  time  in  the  epigas- 
trium. In  addition  to  these  phenomena,  a  third  sound  was 
audible  over  a  small  area  just  internal  to  the  apex  when  in 
the  recumbent  attitude,  not  when  erect.  This  was  of  right 
ventricular  origin. 

Some  six  months  later,  the  heart  was  in  much  the  same 
condition,  except  that  the  apex  was  4  inches  from  the  sternum 
instead  of  3  inches,  and  the  apex  beat  could  be  felt  in  the 
fifth  interspace  when  the  bo}'  was  lying  down.  He  was  much 
stronger  and  better,  but  not  so  well  as  he  would  have  been  had 
he  been  made  to  take  more  rest  and  less  exertion. 

Another  simple  case  of  this  same  type  of  dilatation  as  the 
result  of  overstrain  is  that  mentioned  at  p.  212. 

The  next  case  is  a  young  man  aged  twenty,  who  came  to 
see  me  in  June  1893,  suffering  from  breathlessness  on  exertion 
and  attacks  of  fainting.  He  was  decidedly  anaemic,  and  was 
so  breathless  on  exertion  that  he  could  not  walk  more  than  a 
mile  or  two  quietly,  and  could  not  run  at  all.  He  had  a  little 
pain  in  the  chest  just  above  the  left  nipple  if  he  overtaxed  his 
heart.  He  was  engaged  in  a  flour-mill,  and  had  strained  his 
heart  by  dragging  heavy  bags  of  flour  about.  The  neck 
veins  were  rather  full  with  fluttering  false  pulsation  in 
them.     The  heart  was  very  greatly  enlarged,  and  there  was 


31 1 


THE  HEART  IN  OVERSTRAIN 


well-marked  cardiac  pulsation  fi'om  the  second  to  the 
fourth  interspaces  as  far  as  the  left  nipple  line,  but  none 
to  the  right  of  the  sternum  or  in  the  epigastrium,  though 
there  was  a  httle  relative  dullness  in  the  fourth  right  inter- 
space. The  area  of  cardiac  dullness  was  as  follows :  When 
in  the  erect  attitude  there  was  relative  dullness  in  the  second  left 
interspace  for  If  inches,  and  well-marked  pulsation  for  1  inch 
from  the  sternum.     In  the  third  and  fourth  there  were  4  inches 

Upward  Dilatation  of  the  Heart  in  Overstrain 


Area  of 

loudness 

sound 


Fig.  118. 

John  M.,  aged  twenty,  Jiine  19, 
1S93.  Heart  when  recumbent 
showing  extreme  upward  dilatation, 
but  no  pulmouarj-  murmur. 


Fig.  119. 

Jolm  M.,  June  19, 1S93.  Showing: 
Icfwened  amount  of  upward  dilatation 
when  erect,  with  no  change  in  the 
situation  of  the  apex. 


of  relative  dullness  with  pulsation  over  most  of  this  area.  The 
apex  was  in  the  fourth  interspace,  4  inches  from  the  sternum 
— i.e.,  more  than  1  inch  outside  the  nipple  line.  The  maximal 
beat  of  the  right  ventricle  was  felt  in  the  fourth  interspace  in 
the  nipple  hne,  3  inches  from  the  sternum.  When  this  patient 
lay  down,  the  resulting  relaxation  of  the  anterior  wall  of  the 
right  ventricle  caused  a  marked  upward  increase  in  the  amount 
of  dullness,  for  the  cardiac  dullness  was  now  well  marked  in 
the  first  interspace  extending  1|  inches  out  from  the  sternum, 
and  in  the  second  interspace  the  cardiac  dullness  reached  to 
the  nipple  line  and  there  was  an  inch  of  absolute  dullness 
(vjWfifigs.  118  and  119). 


THE  HEART  IN  OVERSTRAIN  315 

The  interesting  point  about  this  case — in  addition  to  the 
somewhat  extreme  degree  of  upward  dilatation  of  the  right 
ventricle — was  the  complete  absence  of  any  pulmonary  sj-s- 
tolic  murmur.  The  heart  here  was  certainly  strong  enough 
to  produce  one,  as  was  evidenced  by  the  extreme  amount 
of  dilatation  of  the  right  ventricle,  and  also  by  an  extremely 
loud  pulmonary  second  sound.  There  was  great  upward 
displacement  of  the  origin  of  the  pulmonary  artery,  as  was 
shown  by  the  fact  that  the  point  of  maximal  loudness  of  the 
pulmonary  second  sound  was  in  the  first  interspace,  and, 
therefore,  the  pulmonary  valves  were  above  the  level  of  the 
second  rib  instead  of  at  the  level  of  the  third.  Under  such 
circumstances  there  ought  to  have  been  a  very  loud  pulmonary 
systohc  murmur,  and  the  reason  for  there  being  none  must  be 
found  in  the  fact  that  the  pulmonary  orifice  was  dilated  as  well 
as  the  pulmonary  artery,  and,  therefore,  no  murmur  was  caused 
in  the  dilated  artery. 

In  this  case  of  overstrain,  we  see  the  typical  appearances 
of  a  dilatation  of  the  anterior  wall  of  the  right  ventricle,  such 
as  is  described  in  the  essay  on  Anaemia. 

Four  months  later,  the  heart  still  showed  much  dilatation 
upwards,  for  there  was  still  1|  inches  of  relative  dullness  and 
some  pulsation  in  the  second  interspace,  2  inches  in  the  third, 
and  3  inches  in  the  fourth  ;  but  the  amount  of  dullness  was  not 
materially  increased  when  the  patient  lay  down,  although  the 
amount  of  pulsation  in  the  second  interspace  was  increased. 
This  showed  an  increase  in  the  firmness  and  strength  of  the 
anterior  wall  of  the  right  ventricle.  The  apex,  too,  was  lower, 
and  was  felt  in  the  fifth  interspace  when  standing  up,  though 
it  retreated  behind  the  fifth  rib  when  he  lay  down — showing  a 
shght  upward  shift  of  the  whole  heart  with  the  change  of  atti- 
tude. The  point  of  maximal  intensity  of  the  pulmonary 
second  sound  was  still  in  the  first  interspace,  and  there  was  still 
no  pulmonary  systohc  murmur.  The  patient  was  much  better 
and  stronger. 

The  following  case  shows  well  how,  in  early  life,  the  right 
ventricle  dilates  as  a  result  of  overstrain,  although  it  is  a  case 
where  the  heart  was  not  normal,  but  was  so  far  weakened  as 
a   result    of   rheumatism   that    the   intraventricular   pressure 


316  THE  HEAHT  IN  OVERSTRAIN 

necessary  to  cany  on  the  circulation  as  the  patient  was  lying 
in  bed  sufficed  to  cause  the  dilatation. 

The  patient,  a  youth  of  seventeen,  was  admitted  to  the 
General  Hospital,  August  12, 1892,  suffering  from  a  slight  attack 
of  rheumatism,  which  rapidly  yielded  to  treatment  wath  sodium 
salicylate.  There  was,  on  admission,  a  loud  mitral  systolic 
murmur  with  some  dilatation  of  the  left  ventricle,  the  apex 
being  just  outside  the  nipple  line.  There  was  a  slight  amount  of 
enlargement  to  the  left  in  the  third  interspace,  but  no  pulmo- 
nary murmur.  Five  days  later,  the  pulse-rate  dropped  to  forty, 
became  very  soft,  the  cardiac  sounds  lessened  in  loudness,  and 
the  slight  amount  of  dilatation  that  was  present  on  admission 
disappeared,  the  heart  being  of  normal  size.  These  signs  all 
pointed  to  the  onset  of  myocardial  weakness.  Two  daj^s  later, 
with  a  return  of  cardiac  strength,  another  type  of  dilatation 
appeared — namely,  the  upward  enlargement  of  the  right  ven- 
tricle, as  in  the  other  cases  noted.  There  was  relative  dullness 
for  1  inch  from  the  sternum  in  the  second  left  interspace,  and  for 
2  inches  in  the  third,  and  the  apex  was  internal  to  the  nipple  line 
in  the  fifth  interspace.  There  was  visible  and  palpable  pulsa- 
tion in  the  second  and  third  interspaces.  The  apical  murmm* 
was  no  longer  present,  but  there  was  a  well-marked  pulmonary 
systolic  murmur  heard  loudly  both  to  right  and  left  of  the 
sternum  in  the  second  interspaces.  There  was  also  a  faint 
tricuspid  systolic  murmur.  For  more  than  a  week  the  dilata- 
tion and  the  murmurs  remained  well  marked  or  slightly  in- 
creased, and  then  a  fortnight  after  its  sudden  onset,  the 
dilatation  began  to  subside,  and  the  patient  was  discharged  in 
a  few  weeks'  time  with  a  heart  apparently  normal. 

This  is  a  type  of  case  which  can  extremely  often  be  observed 
in  rheumatism  or  other  infective  diseases,  but  it  is  very  instruc- 
tive as  showing  how  the  heart  sometimes  dilates  with  the  retmii 
of  strength  which  follows  myocardial  weakness. 

OvERSTEAiN  IN  Adult  Life. — The  following  is  an  ordinary 
case  of  overstrain  occurring  in  a  healthy  adult,  and  resulting 
in  the  ordinary  adult  type  of  dilatation  of  the  right  ventricle 
as  well  as  of  the  left  {ride  figs.  120,  121,  122). 

The  case  is  as  follows  :  John  W.,  a  man  of  about  forty  years 
of  age,  was  taking  a  holiday  in  Switzerland,  and  on  two  occa- 


THE  HEART  IN  OVERSTRAIN 


317 


sions — once  when  walking  up  to  8t.  Beatenberg,  and  once 
when  walking  up  to  ]\Iurien — had  attacks  of  pain  in  the  neck 
witli  some  breathlessness.  He 
found  that  the  attack  passed 
off  quickly  if  he  stopped  and 
took  deep  breaths,  but  on 
the  way  up  to  Murren,  he 
had  to  stop  thus  a  dozen 
times  or  so.  For  some  weeks 
after  his  return  home,  he 
noticed  that  he  was  gradually 
getting  less  able  to  hurr}^  or 
to  go  upstairs  quickly,  and 
at  the  end  of  September,  he 
was  so  alarmed  at  his  in- 
ability (owing  to  l)reathless- 
ness  and  a  sense  of  powerless- 
ness)  to  saw  through  a  bit  of 
deal  '  only  3|  by  2|  inches  ' 
that  he  came  to  consult  me. 

On   examination,   he  ap- 
peared   well    nourished    and 

fairly  healthy  looking,  but  there  w^as  evident  cardiac  dilatation. 
The  veins  of  the  neck  were  rather  full,  and  there  was  well- 


reA  of 
'pulsation 
standing' 


Fig.  120. 

Jolm  W.,  aged  forty,  September  28,  189G. 
Showing  area  of  cardiac  dullness  and  pulsation. 
The  dotted  area  shows  epigastric  pulsation  only 
observable  when  erect. 


Fig.  121. 

John  W.,    October  6,  189C. 
After  resting. 


Fig.  122. 

John  W.,  October  20,  1896. 
Increase  in  the  area  of  pulsa- 
tion (sho\Mi  by  dots)  after  phy- 
sical and  mental  exertion. 
Cardiac  dullness  much  the 
same. 


marked  visible  and  palpable  true  pulsation  in  them.  The  radial 
pulse  w^as  regular — eighty  to  the  minute — but  small  and  of  rather 
low  tension.     There  was  visible  cardiac  pulsation  in  the  third, 


318  THE  HEART  IN  OVERSTRAIN 

fourth,  and  Hfth  left  interspaces  and  to  the  right  of  the  sternum, 
over  the  area  shown  in  lig.  120,  and  when  he  was  standing  up 
there  was  well-marked  epigastric  pulsation  as  well.  The  apex 
was  low  down  in  the  fifth  interspace  in  the  nipple  line.  Its 
beat  was  feeble  and  wanting  in  vigour,  and  the  left  ventricle 
heart  sounds  also  were  short  and  wanting  in  tone.  There  was 
no  murmur  audible  anywhere,  and  the  right  ventricular  sounds 
Avere  of  better  tone  than  the  left,  and  the  pulmonary  second 
sound  was  rather  accentuated. 

This  condition  improved  somewhat  under  treatment,  but 
he  would  not  take  absolute  rest,  consequently  the  heart  re- 
mained in  an  irritable  condition,  and  dilated  very  easily  as  the 
result  of  physical  and  mental  work,  as  may  be  seen  by  com- 
paring lig.  121  with  %.  122.  It  was  not  until  he  remained 
a  fortnight  in  bed  that  the  heart  returned  to  its  normal 
size,  and  began  really  to  regain  its  strength,  but  it  was  some 
months  before  he  was  able  to  do  a  full  day's  work. 

The  following  is  a  case  of  overstrain  in  which,  owing  probably 
to  relative  weakness  of  the  left  ventricle,  the  resulting  dilatation 
mainly  involved  the  right  side  of  the  heart.  The  case  is  of 
interest  because,  in  spite  of  marked  fullness  of  the  veins, 
some  tricuspid  regurgitation  and  upward  dilatation  of  the 
right  ventricle,  accompanied  by  a  pulmonary  systoUc  murmm*, 
there  was  no  increase  in  the  cardiac  dullness  to  tlie  right  of 
the  sternum,  although  there  w^as  some  pulsation  to  be  felt  in 
that  situation.  Another  point  of  interest  is  that  the  venous 
over-distension  appears  to  have  caused  so  much  increase 
in  the  thoracic  contents  that  the  diaphragm  assumed  a  lower 
le\'el  than  normal,  for  the  line  of  the  liver  dullness  was  an 
interspace  too  low.  The  apex  beat  also  was  in  the  sixth 
interspace  instead  of  the  fifth,  when  the  patient  stood  up,  and 
the  pulsation  of  the  right  ventricle  in  the  epigastrium  was 
abnormally  distinct  when  he  was  in  the  erect  attitude. 

The  patient  was  a  man,  B.  W.,  aged  thirty-seven,  Avho  came  to 
me  in  June  1911,  complaining  of  breathlessness,  irregular  action 
of  the  heart,  and  some  pain  in  the  chest — apparently  of  cardiac 
origin.  There  was  a  history  of  his  having  strained  his  heart 
while  bicycling  eleven  years  ago.  Bmce  then,  he  had  been  well 
enough  to  play  tennis  and  be  a  first-rate  player,  but  he  had  to 


THE  HEART  IN  OVERSTRAIN 


319 


wJzen 


be  careful  about  continuous  exercise — such  as  running.  There 
was  a  recent  history  of  nervous  overstrain,  owmg  to  ditticulties 
in  liis  work — he  was  manager  of  a  brewery,  and  the  badl}^ 
ripened  barley  (due  to  the  last  season's  wet  summer)  caused 
much  trouble  and  anxiety.  About  two  months  prior  to  being 
seen  by  me,  he  had  begun  to  get  unduh^  nervous,  the  pulse  at 
times  running  up  to  over  one  hundred,  and  the  attack  being 
accompanied  by  faintness.  He  then  had  an  attack  of  acute 
indigestion  —  apparently     a 

true  gastralgia  or  a  con-  Low  Diaphragm  in  Case  of  Over- 
,.  ^        ,  1  strained  Heart 

tmuous      transverse      colon 

pain,  which  was  not  made 
worse  by  food  or  by  exertion, 
and  was  relieved  by  rest  and 
milk  diet.  AVhile  still  on 
milk  diet,  he  played  in  one 
w^eek  two  long  and  closely 
fought  tennis  matches,  for 
which  he  had  not  sufficient 
strength,  and  began  to  suffer 
from  breathlessness,  cardiac 
irregularity,  and  some  car- 
diac pain  over  the  apex  of 
the  heart.  He  was  a  healthy 
looking,  well  -  built  man. 
When  standing,  there  was 
well-marked  high  pressure 
pulsations  in  the  veins  just 
above  the  clavicles,  which 
could  be  felt  to  stop  short 

at  the  venous  valves.  There  was  also  some  excessive 
arterial  pulsation  in  the  neck,  but  its  type  and  its  amount 
did  not  suggest  aortic  disease.  The  cardiac  impulse  could 
be  felt  too  forcibly  over  the  lower  end  of  the  sternum  and 
in  the  epigastrium,  also  just  to  the  left  of  the  sternum  in  the 
fourth  and  fifth  interspaces,  and  just  to  the  right  of  the  sternum 
under  the  fifth  and  sixth  ribs.  The  right  ventricular  sounds 
were  also  loud  and  good,  and  there  was  a  distinct,  but  locahsed, 
systoHc  tricuspid  murmur,  and  also  a  well-marked  pulmonary 
murmur,  although  there  was  no  upward  increase  of  the  heart 
into  the  third  and  second  left  interspaces.  On  lying  down 
the  epigastric  impulse  nearly  disappeared,  the  tricuspid  systolic 
murmur  became  louder,  and  well-marked  systolic  pulsation  was 


B. 


Fig.  123. 

W.,  aged  tliirty-seven.  Overstrain  with 
feeble  left  ventricle  and  stronger  and  dilated 
right  ventricle.  Diaphragm  low,  probably  from 
venous  engorgement  of  liuigs. 


320  THE  HEART  IN  OVERSTRAIN 

visible  in  the  neck  veins  nearly  to  the  angle  of  the  jaw.  The 
pulse  was  fairly  strong  and  its  tension  too  liigh.  The  sphj'gmo- 
manometer  showed  a  blood  pressure  of  160  mm.  of  mercury, 
and  at  140  mm.  the  pulse  became  quite  full  and  strong.  The 
left  ventricle  was  somewhat  feeble,  both  as  regards  its  impulse 
(which  could  be  barely  felt)  and  also  its  sounds,  which  were 
weak  and  accompanied  by  a  faint  mitral  systolic  murmur. 
The  apex  was  too  low,  being  in  the  sixth  interspace  when  he  was 
standing,  and  low  in  the  fifth  when  he  lay  down.  There  was 
also  some  dilatation,  for  the  outer  border  of  the  relative  cardiac 
dullness  was  an  inch  external  to  the  nipple  line — 4  inches  from 
mid-sternum.  The  situation  of  the  heart  pointed  to  its  being 
displaced  downwards  by  lowness  of  the  diaphragm  {vide 
fig.  123). 

The  after-history  of  the  case  was  uneventful,  and  the 
heart  gradually  regained  its  strength  under  proper  treatment. 
Within  a  month  the  left  border  of  the  heart  had  come  in 
1  inch,  the  apex  being  in  the  nipple  line  instead  of  an  inch 
external  to  it. 

Overstrain  in  Later  Life. — The  following  is  a  somewhat 
extreme  case  of  dilatation,  the  result  of  continuous  over- 
exertion, in  a  lady  of  eighty-one,  whose  nervous  energy  was  in 
excess  of  the  muscular  power  of  her  heart.  I  was  asked  to 
see  her  after  a  four  hours'  railway  journey  on  account  of  some 
breathlessness  and  faintness. 

She  was  rather  stout,  but  was,  on  the  whole,  wonderfully 
active  both  in  mind  and  body  for  her  age,  and  I  was  surprised 
on  examining  the  heart  to  find  what  an  extreme  degree  of 
dilatation  existed.  There  was  cardiac  dullness  for  more  than 
3  inches  to  the  right  of  the  middle  line,  and  for  7  inches  to  the 
left,  the  apex  of  the  heart  being  in  the  seventh  interspace  in  the 
anterior  axillary  line.  The  transverse  diameter  of  the  heart 
in  this  case  must,  therefore,  have  been  well  over  10  inches, 
which  showed  extreme  dilatation,  considering  that  the  patient 
was  not  (in  spite  of  her  stoutness)  much,  if  at  all,  above  the 
normal  as  regards  height  and  build.  In  spite  of  this  extreme 
dilatation  the  heart  sounds  were  fairly  loud  and  good,  and  there 
was  no  murmur  present  except  the  one  described  at  p.  44  as 
the  superior  vena  cava  murmur.  This  murmur  was  only 
audible  to  the  right  of  the  middle  line,  up  and  down  over  (and 
just  to  the  right  of)  the  right  border  of  the  sternum  from  the 


THE  HEART  IN  OVERSTRAIN 


321 


neck  to  the  fifth  interspace.     The  size  and  shape  of  the  heart  is 
shown  in  the  accompanying  figure  (fig.  124)  which  shows  the  ex- 


KL.y 


Fig.  124. 


Mrs.  W.,  aged  eighty-one.       Extreme  dilatation  of  heart  from  over-activity. 
No  murmur  except  a  suijerior  vena  cava  one. 

treme  size  that  was  observed.     The  heart  in  this  patient  had  lost 
so  little  of  its  elasticity,  that  a  few  days  of  absolute  rest  in  bed 


(=  nearly  4" from, 
mid.  line) 


''■'^^ZofaJbs. 
dulness 


Fig.  125. 

Mrs.  AV.,  aged  eighty-one.    Showing  great  increase  in  dilatation  caused  by  a 
little  more  exertion  than  the  heart  would  stand. 

would  reduce  its  size  and  the  amount  of  pulsation  considerably. 
For  instance,  after  walking  a  dozen  paces  to  and  from  the  lift, 


322  THE  HEART  IN  OVERSTRAIN 

and  spending  the  morning  downstairs  in  a  wheeled  chair,  the 
heart  in  the  afternoon  would  show  (as  in  the  figure)  2  inches  of 
relative  dullness  in  the  second  right  interspace,  and  nearly 
3  inches  to  the  right  in  the  lower  interspaces — i.e.  nearly  to  the 
right  nipple  hne  {vide  fig.  125).  There  would  be  pulsation  to  the 
right  of  the  sternum,  and  the  cardiac  dullness  would  be  nearly 
absolute  just  at  the  right  border  of  the  sternum.  To  the  left  there 
would  be  absolute  cardiac  dullness  in  the  third  interspace  for 
2  inches,  and  relative  dullness  to  the  left  nipple  hne  with  well- 
marked  pulsation.  After  a  few  days'  rest,  the  heart's  apex 
would  come  in  half  an  inch  or  so,  the  pulsation  and  absolute 
dullness  would  be  no  longer  noticeable  in  the  third  left  inter- 
space, and  the  dullness  and  pulsation  to  the  right  of  the  sternum 
would  lessen. 

If  this  patient  had  had  proper  advice  years  before  and 
been  willing  to  follow  it,  most,  if  not  all,  of  this  dilatation 
might  have  been  prevented,  for  there  was  in  all  probabihty  no 
valvular  disease,  although  the  absence  of  valvular  mm-mm-s 
could  not  be  taken  as  certain  evidence  of  this.  It  is  not  possible 
to  say  that  there  was  no  functional  mitral  regurgitation  present. 
It  is  quite  clear  in  this  case — as  shown  by  the  presence  of 
the  superior  vena  cava  mm-mur  and  pulsation  of  the  veins 
in  the  neck — that,  as  might  be  expected,  well-marked 
tricuspid  regurgitation  was  present  in  spite  of  the  absence 
of  any  valvular  tricuspid  regurgitant  murmur.  The  same 
physical  causes  that  prevented  the  development  of  a  tricuspid 
regm-gitant  murmur  (ui  spite  of  the  presence  of  free 
regurgitation)  may  also  have  prevented  the  development 
of  a  mitral  regurgitant  murmur,  in  spite  of  the  presence  of 
free  mitral  regurgitation.  In  cases  of  extreme  enlargement 
of  the  left  ventricle,  we  do  sometimes  find  (as  in  this  case) 
that  there  is  no  systolic  murmur  audible,  although  the  amount 
of  dilatation  makes  it  practically  certain  that  the  valve  must 
be  incompetent.     Such  a  case  is  also  recorded  at  p.  281. 

Extreme  Dilatation  in  Adolescence. — Finally,  I  will 
here  give  a  case  of  overstrain  of  the  right  ventricle  alone  in 
a  girl  of  sixteen,  due  to  extensive  inflammation  of  both  lungs, 
the  result  of  pyaemia  {vide  fig.  126). 

A  neglected  otitis  media  was  the  cause  of  her  pysemia, 
and  when  I  saw  her,  on  October  24,  1898,  three  days  after  her 


THE  HEAET  IN  OVERSTRAIN 


323 


admission  to  the  surgical  wards  of  tho  hospital,  the  heart  was 
enormously  dilated — as  is  shown  in  the  accompanying  diagram. 
There  was  pulsation,  and  1  inch  of  relative  dullness  in  the  first 
left  interspace.     In  the  second  interspace,  the  dullness  and 
pulsation  extended  to  beyond  the  left  nipple  line,  and  in  the 
third  and  fourth  interspaces  to  the  anterior  axillary  line,  some 
5|  inches  from  the  sternum,  and  absolute  dullness  reached  up 
to  the  third  rib.     To  the  right  there  was  relative  dullness  and 
pulsation  for  1  inch  to  the  right  of  the  sternum  in  the  third  and 
fourth  right  interspaces,  giving  a  total  width  of  the  cardiac 
area  of  more  than  7  inches. 
There      was     a      pulmonary 
systolic  murmur  heard   over 
a  small  area  in  the  first  and 

second  left  interspaces,  but  ivf  /k^^^^^^^^^^uX  V^^f^"^" 
no  other  murmur  was  to  be  /^  A  v5^^^^[/i^^fflj^ 
heard.  Next  day,  although 
the  cardiac  dullness  remained 
the  same  to  the  left  of  the 
sternum,  a  pulmonary  mur- 
mur was  no  longer  audible, 
and  the  dilatation  to  the 
right  of  the  sternum  was  less, 
being  only  |  inch  in  wadth. 
The  disappearance  of  the  pul- 
monaiy  murmur,  coinciding 
with  a  lessening  of  the 
amount  of  dilatation  of  the 
heart    to    the    right    of    the 

sternum,  is  confirmatory  of  the  explanation  given  at  p.  275 
as  to  the  absence  of  the  pulmonary  murmur  in  cases  of 
extreme  dilatation,  for  it  suggests  a  shght  gain  in  the 
efficiency  of  the  right  ventricle,  and  such  a  slight  rise  in 
the  intraventricular  pressure  as  might  well  have  caused  a 
dilatation  of  the  pulmonary  orifice,  sufficient  to  cause  the 
disappearance  of  the  murmur. 


Fig.  126. 

Extreme  dilatation   of   heart  in  pyrrmic 
pneumonia. 


This  is  the  case  spoken  of  at  p.  7  in  which,  at  the  post- 
mortem examination  a  day  or  two  later,  the  heart  was  described 
as  of  normal  size,  but  where  a  closer  examination  showed 
that  the  walls  of  the  right  ventricle  and  right  auricle  were 
both  very  thin  and  very  distensible. 

Y  2 


324  THE  HEART  IN  OVERSTRAIN 

Anomalous  Case  of  Overstrain. — The  following  is  a 
somewhat  unusual  and  interesting  case,  because  the  overstrain 
caused  heart  weakness  and  tachycardia  of  a  lasting  description, 
and  not  simply  dilatation  as  is  usual.  The  cardiac  injury 
was  a  result  of  the  combined  nervous  and  physical  overstrain 
accompanying  an  accident,  and  it  raises  some  interesting 
questions  in  connection  with  the  pathology  of  tachycardia. 

The  accident  was  as  follows : — 

The  patient  (a  man  aged  about  thirty,  a  coal-miner  l)y 
occupation)  was  sitting  on  the  front  of  a  full  coal-tub,  which 
was  running  down  towards  the  shaft  along  a  10  feet  wide 
'  road,'  when  it  suddenly  ran  off  the  rails,  and  he  had,  by 
a  violent  effort,  to  jump  off  the  tub  sideways  in  order 
to  save  his  life.  The  tub  ran  into  the  wall  and  knocked 
the  roof-props  dovm,  and  the  roof  of  the  passage  fell  in.  The 
suddenness  of  his  jump  put  his  own  lamp  out,  and  he  had  to 
sit  in  darkness,  hearing  the  roof  falling  in  all  round  him,  and 
expecting  every  moment  to  be  crushed  to  death.  He  had  to  sit 
thus  for  ten  minutes  before  he  was  rescued  from  his  dangerous 
position. 

Although  the  sudden  effort  of  the  jump  for  his  hfe  was  not 
calculated  to  cause  any  severe  cardiac  damage,  the  prolongation 
of  the  state  of  strain  by  the  nerve  shock  which  followed  it  seems 
to  have  been  sufficient  to  cause  very  severe  damage.  An 
additional  reason  for  the  severit}^  of  the  cardiac  overstrain  may, 
I  think,  be  found  in  the  following  considerations  :  The  sudden 
violent  effort  caused  a  sudden  violent  action  of  the  heart. 
Under  ordinarj^  circumstances  this  would  have  done  no  damage, 
as  the  heart  would,  in  a  few  seconds,  have  returned  to  its  normal 
mode  of  beating.  The  occurrence,  however,  of  fear  kept  up 
the  overaction  of  the  heart  for  several  minutes,  and  led  to  an 
amount  of  overstrain  that  did  cause  damage  to  the  heart. 

I  first  saw  the  man  more  than  three  years  after  the  accident, 
and  he  was  then  incapacitated  from  work,  l)ecause  of  palpita- 
tion, pain,  and  breathlessness.  There  was  then  no  cardiac 
dilatation,  and  the  physical  signs  suggested  muscular  weakness 
of  the  heart  involving  the  left  side  more  than  the  right.  The 
pulse-rate  was  over  110  on  slight  exertion,  but  after  a  few 
minutes'  rest  would  drop  to  90.  Slight  exertion  would  cause 
the  appearance  of  right  ventricular  pulsation  to  the  left  of  the 
sternum,  and  it  is,  therefore,  probable  that  both  his  pain  and 


THE  HEART  IN  OVERSTRAIN  325 

his  breathlessness  were  due  to  the  over-distension  of  the  right 
ventricle,  which  resulted  from  its  attempt  to  compensate  for 
the  inability  of  the  left  ventricle  to  meet  the  call  for  increased 
work  during  muscular  activity. 

An  interesting  question  raised  by  this  case  is  the  following : 
What  part  did  '  tachycardia  '  play  in  the  cardiac  disability 
of  this  patient  ?  To  make  my  meaning  clear,  I  will  give  an 
illustration  of  a  different  kind.  A  lady  was  walking  along  a 
road  where  some  boys  are  playing  with  a  football.  She  was 
suddenly  struck  a  severe  blow  on  the  side  of  the  head  by 
the  football  ;  moreover,  as  it  was  kicked  from  behind  her, 
she  could  not  see  it  coming,  and,  therefore,  nervous  shock 
due  to  sudden  fright  accompanied  the  physical  shock  of  the 
blow.  The  result  was  that  the  sudden  powerful  contraction 
of  the  neck  muscles,  wliich  was  necessary  to  prevent  damage 
to  the  cervical  spine,  instead  of  being,  as  might  be  expected, 
a  single  contraction,  was  perpetuated  as  a  clonus  of  the  neck 
muscles,  and  spasmodic  torticollis  resulted.  I  saw  the  patient 
a  few  weeks  afterwards,  and  she  was  then  a  typical  case  of 
severe  spasmodic  torticoUis.  The  habit  of  clonic  spasm, 
started  by  the  accident,  had  become  firmly  established,  and 
it  took  many  months  of  most  assiduous  exercises  before  the 
habit  could  be  broken,  and  it  was  two  years  before  the  patient 
was  reasonably  free  from  clonic  spasm  of  the  neck  muscles. 

The  question  now  arises  :  How  far  was  the  irregular 
action  of  the  heart  in  the  case  of  the  miner  due  to  the 
sudden  and  violent  jump  for  hfe,  and  then  the  keeping 
up  of  the  rapidity  for  ten  minutes  by  the  terror  of  that 
time  of  waiting  in  the  dark  with  the  roof  of  the  passage 
continually  falling  in  around  him  ?  It  is  probable  that 
there  was  both  physical  strain  with  damage  to  some  of  the 
cardiac  fibres  combined  with  what  may  be  called  habit  tachy- 
cardia. When  he  came  under  my  care,  three  years  after  the 
accident,  he  was  admitted  into  hospital,  and  kept  quiet  in 
bed  without  any  treatment  directed  to  the  heart,  except  a 
little  nickel  sulphate.  The  heart's  rate  gradually  came  down, 
and  after  some  weeks,  when  he  was  gradually  allowed  to 
resume  a  certain  amount  of  activity,  the  tachycardia  did  not 
return.     He  gradually  improved  after  tliis — finding  that  the 


326 


THE  HEART  IN  OVERSTRAIN 


amount  of  work  ho  was  able  to  do,  without  causuig  a  return 
of  the  rapidity,  steadily  increased,  but  even  after  the  lapse  of  a 
year  the  pain  and  rapidity  would  return  as  a  result  of  too 
much  digging  in  his  garden,  or  of  walking  uphill,  and  anything 
approaching  ordinary  manual  labour  was  still  out  of  the 
question.  A  few  notes  as  to  his  condition  after  the  accident 
and  on  admission  to  hospital  two  years  later  may  be  of  interest. 

After  the  accident,  he  did  not  notice  any  pain  in  his  chest 

for    the    first    three 
days.      Three    days 
after    the    accident, 
he    began    to    have 
pain  in  the  precordial 
'^d^r^^^iy   region,  but,  in  spite  of 
-  =%^3%,'  its  gradually  getting 
^1>  worse,   he    went   on 

working  for  a  month, 
when  it  got  so  bad 
that  he  had  to  give 
up.  He  describes 
the  pain  as  starting 
in  the  left  axilla 
about  the  sixth  inter- 
costal space,  and 
shooting  up  to  the 
shoulder.  On  reach- 
ing the  shoulder,  the 
pain  would  radiate 
out  over  the  neck,  giving  a  sensation  like  electricity.  The 
pains  would  usually  come  on  when  he  sat  down  after 
exertion  rather  than  during  its  continuance.  The  pains  were 
accompanied  by  dyspnoea.  At  the  time  of  his  admission 
to  the  General  Hospital,  three  years  after  the  accident, 
he  was  still  liable  to  have  shoots  of  pain  as  above  described, 
lasting  two  or  three  minutes,  if  he  overexerted  himself  in  any 
way.  These  shoots  of  pain  seemed  to  be  accompanied  by  such 
forcible  action  of  the  heart  that  the  patient  himself  could 
feel  it  thumping  in  the  chest. 

The  condition  of  the  heart  on  admission  is  shown  by  the  out- 
lines in  fig.  127,  and  also  by  Plate  II,  showing  a  photograph 
of  the  patient  after  the  area  of  heart,  liver,  and  stomach  had 


EiG.  127. 

Thos.  S.,  aged  thirty.  Showiug  high  diaphragm  on 
both  sides,  a  small  heart  dullness,  and  a  lessening  of  the  liver 
dullness. 


PLATE  II 


Photograph  of  the  Patient  Thos.  S.,  showing  the  actuax  Oltline  of  the 
Heart,  Lungs,  and  Stomach  (as  determinable  by  Percussion)  marked  upon 
THE  Chest,  and  also  the  Situation  of  the  Ribs  (marked  in  roman 
numerals)  and  of  the  Costal  Arch  (C.A.). 

Note  the  close  correspoudence  of  the  original  with  the  diagram  shown  in  fig.  127  ;  compare  also  Plate  IV 
with  fig.  130,  p.  36-t.  These  photographs  show  the  excellence  of  the  diagram  of  the  chest  used  in  this 
book.  It  is  printed  by  Messrs.  Danielsson  from  a  drawing  by  Prof.  Luschka,  of  Vienna.  It  is  a 
marvellously  perfect  generalisation,  and  in  the  course  of  nearly  thirty  years'  experience  with  it  the  writer 
has  very  rarely  indeed  found  it  to  be  at  fault.  It  has  proved  invaluable  in  the  clinical  studies  upon 
which  much  of  this  book  is  based. 


I'llOTUCKAPH    OF    ThOS.   S..  SHOWIXO    THE    UUTLINK    UK    THE    \  ISCERA,    AS    .MARKED    OX 

THE  Chest,  as  the  result  of  Percussion. 

This  plate  sliows  the  extension  of  tlie  gastric  resonance  into  the  axilla  where  it  reacheJ  nearly  to  the 
mid-axillary  line  in  the  sixth  interspace. 


THE  HEART  IN  OVERSTRAIN  327 

been  marked  on  the  skin.  These  show  the  diaphragm  to  be  high 
and  the  liver  dullnesss  to  be  small.  Moreover,  the  smallness 
of  the  stomach,  combined  with  the  high  diaphragm,  cause  rather 
a  remarkable  shifting  of  the  gastric  resonance  towards  the  axilla. 
This  is  well  shown  in  the  photograph  (Plate  III).  Note  the 
height  of  the  relative  liver  dullness  on  the  right  side,  the  broad- 
ness of  the  area  between  the  absolute  and  relative  dullness, 
showing  abnormal  arching  of  the  diaphragm.  Note  also  the 
distance  that  the  lower  border  of  the  liver  dullness  is  from  the 
costal  arch,  suggesting  not  only  a  drawing  up  of  the  organ  by  the 
abnormal  rise  of  the  diaphragm,  but  also  probably  a  true  dimi- 
nution in  its  size,  from  its  being  underfilled  with  blood  in  common 
with  the  thoracic  viscera.  Also  note  that  the  amount  of  cardiac 
dullness  in  the  thnd  interspace  is  much  increased  (it  extends 
to  bej^ond  the  nipple  hne).  This  might  be  simply  explained 
by  the  rise  of  the  diaphragm  lifting  the  heart  as  a  whole,  were 
it  not  for  the  fact  that  there  is  an  abnormal  amount  of  pulsation 
in  this  interspace,  which  readily  increases  in  amount  during  any 
excitement,  and  thus  shows  that  some  upward  dilatation  of 
the  right  ventricle  is  present. 

The  pathology  of  such  a  case  as  this  is  not  very  clear.  The 
ordinar}^  explanation  would  be  damage  to  certain  of  the  muscular 
fibres  of  the  heart  as  a  result  of  the  overstrain  ;  but  against  this, 
as  the  prime  factor,  is  the  slightness  of  the  actual  amount 
of  extra  work  that  the  heart  did,  if  it  is  to  be  judged  by  the 
force  put  out  in  the  suagle  jump  for  Hfe.  There  is,  however, 
in  the  case  another  less  evident  cause  of  actual  physical  over- 
strain— namely,  the  one  that  is  so  apt  to  cause  the  death  of 
persons  with  weak  hearts  after  running  to  catch  a  train.  Any- 
one who  has  tried  the  experiment  of  sitting  absolutely  still  after 
the  sudden  cessation  of  violent  exertion — such  as  running  fast 
up  a  hill  or  upstairs — will  find  how  greatly  such  an  action 
exaggerates  and  prolongs  the  sUght  dyspnoea,  which  the  exercise 
would  otherwise  have  caused.  The  physiological  reason  for  this 
is  that  durmg  exercise  the  heart  is  pumping  blood  with  full 
force  into  the  muscular  arterioles,  which  are  fully  dilated  in 
response  to  the  functional  activity  of  the  muscles.  With  the 
sudden  cessation  of  functional  activity  there  is  sudden  vaso- 
constriction of  the  muscular  arterioles,  and  the  heart  which  is 


328  THE  HEART  IN  OVERSTRAIN 

fully  distended  with  blood  and  working  at  high  pressure  will  be 
very  greatly  embarrassed  by  the  sudden  closing  up  of  the 
channels  into  which  it  was  about  to  pump  the  blood.  The 
sudden  cessation  of  exertion  in  the  case  of  this  man  as  he  sat 
absolutely  still  in  the  dark  may  have  thrown  some  extra 
strain  upon  the  heart,  but  even  so  it  is  not  easy  to  see  how 
such  a  lasting  damage  could  be  done  to  its  muscular  fibres, 
and  there  is  also  another  point  which  suggests  that  phj^sical 
overstrain  was  not  the  only  or  perhaps  even  the  main  factor 
in  this  case.  Had  muscular  damage  resulted  from  the  accident 
the  symptoms  of  muscular  weakness  surely  ought  to  have 
developed  at  once,  instead  of  gradually,  as  was  the  case.  If, 
however,  tachycardia  played  a  considerable  part  in  the  case, 
the  overstrained  heart  muscle  would  gradually  get  worse — as 
was  the  case  here — owing  to  the  man  attempting  to  go  on  with 
his  work,  in  spite  of  the  rapidity  of  the  cardiac  action. 

The  case  is  an  interesting  one,  and  the  further  light  which 
might  be  thrown  upon  it  by  other  cases  of  a  similar  nature 
would  be  very  desirable.  In  connection  with  this  case  it  is  of 
interest  to  compare  the  case  recorded  at  p.  115,  which  appears 
also  to  have  been  one  of  '  habit  irregularitv  '  of  the  heart. 


Essay  VII.— UPON  DILATATION  OF  THE  EIGHT 
VENTEICLE  i 

The  early  recognition  of  .slight  degrees  of  dilatation  of  the 
right  heart  is  of  such  great  clmical  importance  that  I  need 
say  nothing  h}'  way  of  introduction  to  the  subject  of  which 
I  am  about  to  speak  m  this  essay.  I  propose  to  take  up 
in  detail  the  special  clinical  features  of  dilatation  of  the  right 
ventricle  ;  but  before  doing  so  it  is  necessary  to  say  a  word 
or  two  as  to  the  nature  and  extent  of  this  dilatation  as  seen  in 
the  post-mortem  room. 

Briefly,  post-mortem  study,  both  of  the  flaccid  and  distended 
organ  in  cases  of  failure  of  the  right  side  of  the  heart,  shows 
that  the  main  change  is  an  increase  of  the  right  ventricle 
upwards  and  to  the  left.  This  increase  is  largely  due  to  a  dis- 
tension of  the  conus  arteriosus  and  of  the  part  of  the  anterior 
wall  which  is  adjacent  to  it.  This  upward  increase  may  be  so 
great  that  the  pulmonary  valves  lie  under  the  first  left  interspace 
or  even  under  the  first  rib,  while  to  the  left,  the  ventricle  may 
extend  nearly  or  quite  to  the  nipple  line  in  the  second  left 
interspace.  Increase  to  the  right  of  the  sternum  plays,  as  a 
rule,  only  a  secondary  part  as  compared  with  that  in  an  upward 
direction.  This  statement  holds  true  for  cases  due  to  valvular 
disease  as  well  as  for  those  where  there  is  none. 

Together  with  this  change  there  is  a  displacement  of  the 
whole  heart  upwards  and  some  rotation  of  the  organ,  so  that 
the  left  ventricle  assumes  a  position  rather  more  posterior 
than  normal,  while  the  apex  is  tilted  upwards  and  outwards, 

^  Two  clinical  lectures  delivered  at  the  Birmingham  General  Hospital, 
June  1894  ;  printed  in  the  Lancet,  September  1894,  and  Birmingham  Medical 
Review,  September  1894,  and  reprinted  here  verbatim  with  a  few  omissions. 

[This  essay,  which  was  written  twenty  years  ago,  gives  a  useful  summary 
of  much  that  is  siid  at  greater  length  in  Essay  I  and  Essay  V.] 

329 


330  DILATATION  OF  THE  RIGHT  VENTRICLE 

and  is  often  brought  into  the  fourth  interspace  in,  or  external 
to,  the  left  nipple  line.  These  latter  changes  are  most  evident 
in  cases  where  valvular  disease  is  not  present. 

The  anatomical  considerations  which  determine  the  direc- 
tion in  which  the  right  ventricle  enlarges,  as  well  as  those  which 
determine  the  displacement  of  the  apex  beat,  have  already 
been  discussed  (see  pp.  247-254 ;  where  also  the  valuable  pioneer 
work  done  by  the  late  Dr.  Arthur  Foxwell  upon  this  subject 
is  referred  to). 

The  Physical  Signs  of  Dilatation  of  the  Eight 
Ventricle  are,  to  some  extent,  disguised  or  altered  in  cases 
of  valvular  disease  by  the  changes  in  size  which  the  left  ventricle 
undergoes,  and  therefore,  for  the  sake  of  clearness,  I  shall 
describe  the  physical  signs  of  dilatation  occurring  in  cases 
with  no  valvular  disease — such  as  those  commonly  occurring 
in  ansemia,  chlorosis,  and  overstrain  during  adolescence,  or 
those  occurring  during  convalescence  from  rheumatic  fever 
or  the  acute  stage  of  pneumonia. 

Among  these  cases  of  so-called  functional  dilatation  a 
further  distinction  must  be  made,  because  the  character  varies 
somewhat  according  to  the  period  of  life  and  the  circumstances 
under  which  it  occurs — for  two  slightly  different  types  of 
dilatation  are  recognisable.  These  may  be  called  the  ado- 
lescent and  the  adult  type  respectively. 

Adolescent  and  Adult  Types  of  Dilatation. — In 
the  earlier  periods  of  life,  and  especially  during  puberty  and 
adolescence,  the  heart  is  naturally  less  resistant  and  less  rigid 
than  it  is  later  in  life,  and  is  therefore  more  prone  to  excessive 
degrees  of  dilatation. 

In  the  adolescent  type  of  dilatation,  to  which  my  descriptions 
will  in  the  main  refer,  the  increase  in  size  is  chiefly,  and  often 
exclusively,  upwards  and  to  the  left,  giving  an  increased  area 
of  relative  cardiac  dullness  in  the  third  and  second  left  inter- 
spaces and  sometimes  even  the  first  interspace. 

In  the  adult  type,  on  the  other  hand,  some  increase  of 
the  cardiac  dullness  to  the  right  of  the  sternum  usually 
accompanies  the  upward  increase,  and  may  exceed  it 
in  amount.  I  need  hardly  point  out  that  such  divisions  as 
these  are  not  meant  to  be  mutually  exclusive,  nor  are  they 


DILATATION  OF  THE  RIGHT  VENTRICLE         331 

meant  to  do  moro  than  assist  in  the  mental  classification 
of  clinical  observations.  Neither  do  I  mean  to  imply  that 
the  adult  type  of  dilatation  is  a  type  which  occurs  invariably 
above  the  age  of  twenty-five  or  twenty-six  when  the  right 
ventricle  fails  ;  for  in  the  degenerative  period  of  life  the 
heart  may  be  so  rigid  that  the  patient  may  die  with  failure  of 
the  right  heart,  but  with  scarcely  any  clinically  recognisable 
dilatation  of  the  right  ventricle  ;  or,  on  the  other  hand,  a  man 
of  thirty  or  thirty-five  may  have  his  heart  substance  so 
softened  by  rheumatic  fever  that  his  right  ventricle  may  dilate 
just  as  rapidly  and  extensively  as  in  any  adolescent. 

The  physical  signs  of  the  adolescent  type  of  so-called 
functional  dilatation  of  the  right  ventricle  are  fairly  definite 
and  characteristic. 

Inspection  and  Palpation  of  a  well-marked  case  will  show 
cardiac  pulsation  in  the  second  and  third  left  interspaces  as 
well  as  in  the  ordinary  situation  ;  and  this  pulsation  will  be 
noticed  to  extend  outwards  for  some  1|  or  2  inches  from  the 
sternum  in  the  former,  and  to  the  nipple  line  in  the  latter 
interspace. 

Further,  the  pulsation  is  not  powerful  like  the  apex  beat 
nor  hke  that  of  an  aneurysm  ;  and,  as  was  pointed  out  by  Dr. 
Foxwell  {loc.  cit),  has  a  very  characteristic  wavy  appearance. 
The  wave  of  pulsation  may  be  noted  sweeping  downwards 
and  outwards  from  the  sternal  end  of  the  second  left  interspace. 
This  pulsation  is  often  further  distinguishable  at  a  glance 
from  that  of  aneurysm  by  the  fact  that  w^hen  the  patient  is 
recumbent  the  pulsation  varies  with  respiration,  being  most 
marked  with  the  cardiac  beats  which  occur  during  the  pause 
between  inspiration  and  expiration,  as  well  as  wdth  the  first 
one  to  occur  during  the  latter  act.  That  this  variation  is  not 
due  simply  to  the  position  of  the  lungs  is  shown  by  the  fact 
that  if  the  breath  be  held  at  the  end  of  expiration,  the  pulsation 
is  usually  less  evident  than  during  active  breathing. 

The  pulsation  can  be  recognised  as  being  due  to  the  right 
ventricle,  and  not  the  pulmonary  artery,  by  the  fact  that  it 
completely  subsides  before  the  occurrence  of  the  second  sound. 
The  cardiograph  also  shows  it  to  be  ventricular.  Detectio7i 
of  the  'pulsation,  above  described,  in  the  second  left  interspace 


332  DILATATION  OF  THE  RIGHT  VENTRICLE 

by  ixilfaiion,  together  with  the  displacement  of  the  apex  heat 
upwards  and  outwards,  is  often  all  the  physical  examinatioii 
necessary  for  the  diagnosis  of  a  dilated  right  ventricle. 

Ill  addition  to  this  cardiac  pulsation  there  will  also  usually 
be  noticed  pulsation  in  the  veins  of  the  neck — usually  of 
the  type  called  '  false  pulsation,'  and  occurring  only 
during  inspiration,  and  due  not  to  failure  of  the  valves, 
but  simply  to  the  more  rapid  emptying  of  the  dis- 
tended veins  which  results  from  the  aid  given  by  the 
inspiratory  suction  to  the  forces  which  till  the  right  ventricle 
during  the  cardiac  diastole. 

As  a  result  of  careful  cardiographic  observation,  I  have  every 
reason  to  believe  that  some  of  these  cases  of  false  pulsation 
are  also  largely  due  to  a  true  contraction  of  the  veins  preceding 
and  probably  also  accompaning  that  of  the  auricle. 

Frequently  the  shock  of  the  closure  of  the  pulmonary 
semilunar  valves  can  be  clearly  felt  in  the  second  interspace, 
and  in  extreme  cases  a  true  systolic  thrill,  not  due  to  valvular 
disease,  is  present  in  this  interspace  over  the  pulmonary  artery, 
and  may  even  be  detected  in  the  subclavian  and  carotid  arteries 
on  the  left  side  and  much  less  strongly  in  those  on  the  right, 
just  as  is  the  case  with  the  pulmonary  systohc  murmur  with 
which  the  thrill  is  associated.  Pulsation  may  also  be  noted 
to  the  right  of  the  sternum  and  in  the  epigastrimn,  but  is  less 
marked  as  a  rule  in  either  of  these  situations  than  at  the  base 
of  the  heart  in  the  cases  now  under  consideration. 

The  apex  beat,  as  before  mentioned,  is  rotated  upwards 
and  outwards  so  as  usually  to  reach  a  point  in  the  fourth  inter- 
space in  or  external  to  the  nipple  line,  but  in  consequence  of 
the  size  of  the  right  ventricle  it  is  often  prevented  from  striking 
the  chest  wall  and  may  therefore  be  feebly  perceptible.  The 
most  prominent  point  of  the  cardiac  impulse  is  in  such  a  case 
situated  internal  to  the  nipple  line  and  is  duo  to  the  impact 
of  the  body  of  the  right  ventricle. 

Percussion  of  the  Ventricle. — Although  inspection  and 
palpation  may  suffice  when  dealing  with  a  well-marked  case, 
it  is  upon  percussion,  aided  by  auscultation,  that  we  have  to 
rely  for  the  early  diagnosis  of  dilatation  of  the  right  ventricle. 
Since  the  ventricle  when  slightly  dilated  lies  at  some  distance 


DILATATION  OF  THE  EIGHT  VENTRICLE  333 

from  the  chest  wall  and  is  overlapped  by  lung,  we  must  rely 
upon  the  area  of  relative  cardiac  dullness  for  this  diagnosis  ; 
and,  as  a  matter  of  practice,  better  results  will  be  got  by  watching 
the  relative  rather  than  the  absolute  dullness,  because  the  latter 
frequently  does  not  increase  at  anything  like  the  same  rate 
as  the  former  when  the  ventricle  is  dilating. 

In  ascertaining  the  area  of  relative  dullness  it  is  well  to  do 
away  with  the  uncertainty  arising  from  the  variation  in  volume 
of  the  lungs  by  percussing  the  heart  while  the  chest  is  held 
in  the  position  of  full  expiration,  and  of  course  to  percuss 
with  the  pleximeter  finger  in  line  with  the  interspace  and  not 
across  it.  This  is  my  usual  practice  when  percussing  the  right 
ventricle ;  and  I  find  that  while  by  this  means  a  change  of  note 
can  frequently  be  got  to  the  right  of  the  sternum  in  a  normal 
heart  it  is  very  unusual  to  get  any  distinct  deficiency  of 
resonance  at  the  sternal  end  of  the  second  left  interspace. 

It  must  of  course  be  borne  in  mind  that  the  descent  of  the 
ribs  in  forced  expiration  will  make  the  position  of  the  heart 
appear  higher  relatively  to  them  than  during  ordinary  re- 
spiration. This  alteration  is  not,  however,  as  a  rule,  sufficient 
to  cause  any  relative  cardiac  dullness  in  the  second  left 
interspace  or  to  make  the  apex  beat  disappear  from  the 
fifth  interspace  if  the  heart  be  normal. 

An  important  feature  in  the  percussion  of  these  '  adolescent ' 
cases,  and  one  which  has  important  bearings  upon  the  causation 
of  the  basal  systolic  murmur  of  anaemia  and  debility,  is  the  fact 
that  the  cardiac  dullness  in  the  second  and  third  left  interspaces 
is  increased  when  the  patient  lies  down.  The  difference  is 
often  considerable,  and  there  frequently  is  as  much  as  an  inch 
more  relative  dullness  in  the  second  space  when  the  patient 
is  recumbent  than  there  is  when  in  the  erect  position. 

Percussion  of  the  heart  in  dilatation  of  the  right  ventricle 
shows  that  the  area  of  relative  dullness  increases  upwards  into 
the  second  space  and  broadens  outward  in  the  third  and  fourth 
spaces,  until  in  advanced  cases  the  left  edge  of  the  dullness 
almost  coincides  with  the  left  vertical  nipple  line  from  the  second 
to  the  fourth  spaces  inclusive.  At  the  same  time  there  may 
be  a  slight  increase  of  the  relative  dulhiess  to  the  right  of  the 
sternum,  but  it  rarely  exceeds  one  inch  ;   on  the  other  hand, 


334  DILATATION  OF  THE  EIGHT  VENTRICLE 

there  often  seems  to  be  an  actual  diminution  of  dullness  in 
this  direction.  The  absolute  cardiac  dullness  broadens  and 
also  extends  upwards,  and  may  in  advanced  cases  reach  a 
width  of  one  inch  in  the  second  left  space  ;  it  very  rarely 
extends  to  the  right  of  the  sternum. 

Auscultation. — The  diagnosis  of  dilatation  of  the  right 
ventricle  by  means  of  the  stethoscope  is  not  so  satisfactory  as 
by  the  methods  just  discussed,  for  the  auscultatory  phenomena 
are  not  always  definite  and  constant. 

Among  the  physical  signs  which  may  be  looked  for  are  the 
following  : — 

1.  The  well-known  pulmonary  systoUc  murmui-,  usually 
heard  best  in  the  second  left  interspace. 

2.  Accentuation  of  the  pulmonary  second  sound,  and 
occasionally  true  reduplication  of  the  second  sound  at  the  base 
of  the  heart. 

8.  The  venous  hum,  so  well  known  in  cases  of  anaemia, 
and  called  the  hruit  de  diable. 

4.  The  murmur  due  to  tricuspid  regurgitation. 

5.  Less  frequently  a  false  reduplication  of  the  second  sound, 
audible  only  over  the  ventricle  and  constituting  one  of  the 
varieties  of  hruit  de  galop  or  '  triple  sound.'  This  sound  is 
quite  distinct  in  origin,  in  time,  and  in  area  of  audition  from 
the  second  sound,  and  I  have  for  several  years  called  it  the 
'  third  soimd  '  of  the  heart. 

6.  More  rarely  still  a  tricuspid  diastolic  murmur  accompany- 
ing or  replacing  the  third  sound  above  mentioned. 

1.  The  Pulmonary  Systolic  Murmur. — The  most  reliable 
and  constant  of  the  above-mentioned  phenomena  is  the  well- 
know^n  systolic  murmur  audible  at  the  base  of  the  heart  to  the 
left  of  the  sternum,  and  correctly  designated  the  pulmonary 
systolic  murmur.  This  murmur  is  of  considerable  diagnostic 
value  in  the  dilatation  which  occurs  as  a  result  of  overstrain 
with  or  without  chlorosis  or  anaemia  in  adolescence.  Its 
loudness  may  be  taken  as  a  reliable  guide  to  the  amount  of  the 
upward  enlargement  of  the  ventricle  which  is  present.  A  good 
illustration  of  this  is  the  increase  m  the  loudness  of  the  murmur 
which  accompanies  the  increase  of  the  cardiac  dullness  when 
the  patient  lies  down.     The  murmur  is  also  markedly  increased 


DILATATION  OF  THE  EIGHT  VENTRICLE  335 

by  exertion,  and  this  is  apt  to  lead  to  a  fallacy  in  connection 
with  the  statement  last  made,  for  it  will  be  increased  in  loudness 
by  any  sudden  change  of  position. 

The  above  statement  that  the  murmur  is  proportional 
in  loudness  to  the  degree  of  upward  increase  of  the  dullness 
does  not  always  hold  true  for  acute  cases  occurring  in  pneumonia 
and  alUed  conditions,  for  in  them  the  murmur  may  be  faint 
although  the  amount  of  dilatation  be  considerable. 

Speaking,  however,  of  the  before-mentioned  non- febrile  cases 
of  dilatation  in  adolescents  we  can  say  that  the  pulmonary 
systohc  mm-muris  a  good  indication  of  the  presence  and  amount 
of  dilatation  in  any  particular  case,  and  gives  the  first  sign  of 
commencing  dilatation  and  is  the  last  sign  to  disappear  on  its 
subsidence.  In  slight  cases  it  is  only  audible  when  the  patient  is 
recumbent,  especially  after  considerable  exertion,  and  is  then 
soft  and  faint,  and  its  area  of  audition  is  confined  to  a  small  area 
one  inch  or  so  in  diameter  at  the  sternal  end  of  the  second 
left  interspace.  When  well  marked,  the  mm-mm-  is  blowing  in 
character,  resembling  the  ordinary  mitral  systohc  murmur, 
except  that  the  pitch  of  the  former  is  often  lower,  and  may 
sometimes  be  almost  humming  in  character.  Its  point  of 
maximal  intensity  is  over  the  second  left  interspace,  usually 
at  its  sternal  end,  although  when  the  dilatation  is  considerable 
this  point  may  be  as  much  as  one  inch  or  more  from  the 
sternum. 

Direction  of  Conduction.  —  It  is  conducted  upwards 
and  to  the  left  to  a  greater  extent  than  downwards  and  to  the 
right:  in  fact,  unless  very  loud  it  is  usually  not  heard  below 
the  third  interspace.  When  loud  it  is  audible  into  the  sub- 
clavian and  carotid  arteries,  although  it  is  better  conducted 
to  those  of  the  left  than  those  of  the  right  side.  When  very 
loud  it  is  even  audible  into  the  axillary  arteries  and  over  a 
great  portion  of  the  upper  part  of  the  chest  anteriorly.  It 
may  even  be  accompanied  by  a  distinct  systolic  thrill,  which 
in  extreme  cases  may  be  palpable  over  a  wide  area  and  follows 
the  same  lines  of  conduction  as  the  murmur. 

Etiology  of  the  Pulmonary  Systolic  Murmur. — The 
exact  cause  of  this  murmur  is  not  perfectly  certain,  but  the 
pathological  condition   on  which   it  depends   seems,  as  was 


336  DILATATION  OF  THE  RIGHT  VENTRICLE 

pointed  out  by  Dr.  Foxwell  {loc.  cit),  to  be  the  upward  displace- 
ment of  the  anterior  portion  of  the  root  of  the  pulmonary- 
artery.  In  consequence  of  the  upward  dilatation  and  displace- 
ment of  the  anterior  wall  of  the  right  ventricle,  while  the  inter- 
ventricular septum  which  forms  the  posterior  wall  remains 
fairly  normal,  there  is  some  distortion  of  the  pulmonary  artery. 
This  seems  to  be  of  two  kinds  :  Firstly,  alteration  in  the 
du-ection  of  the  artery  in  relation  to  the  line  of  the  ventricular 
cavity,  in  consequence  of  the  artery  having  to  reach  its  fixed 
point  (namely,  the  bifurcation  of  the  trachea)  from  a  point  under 
the  first  interspace,  instead  of  running  its  usual  course  from 
imder  the  second  interspace  to  the  bifurcation.  Secondly,  a 
potential  redundancy  of  tissue  m  its  anterior  wall.  Normally, 
the  anterior  wall  runs  from  a  point  subjacent  to  the  middle 
of  the  third  costal  cartilage  in  a  curved  course  to  the  point 
where  the  artery  bifurcates  close  to  the  spine — a  distance,  say, 
of  two  inches  and  a  half.  When,  however,  the  right  ventricle 
is  dilated  the  anterior  wall  of  the  artery  commences  at  a  spot 
nearly  an  inch  nearer  to  the  point  of  bifurcation  than  normal, 
while  the  posterior  wall  retains  more  nearly  its  normal  relations. 
The  result  of  this  is  that  when  the  artery  is  full  the  anterior 
wall,  being  somewhat  relaxed,  will  distend  more  easily  than 
is  normally  the  case,  and  therefore  during  each  systole  there 
will  be  formed  an  aneurysm-like  dilatation  of  the  artery.  We 
would  expect  this  bulging  to  be  more  marked  in  the  recumbent 
than  in  the  erect  posture,  because  in  the  latter  case  gi-avitation 
tends  to  prevent  the  heart  from  taking  quite  such  a  high 
position  as  it  would  otherwise  do.  Strong  evidence  in  favour 
of  the  above  theory  is  given  by  the  fact  that  the  murmur 
increases  in  loudness  proportionally  to  the  increase  in  dullness 
which  occurs  when  the  patient  lies  down,  the  murmur  always 
being  louder  when  the  patient  is  recumbent  than  when 
erect. 

According  to  tliis  theory,  the  conduction  to  the  vessels  of 
the  neck  is  of  course  due,  as  was  pointed  out  in  the  paper  above 
referred  to,  to  the  contiguity  of  the  aorta  and  pulmonary 
artery.  If,  post-mortem,  both  sides  of  the  heart  be  distended 
with  hard  paraffin  before  the  removal  of  the  heart  and  lungs 
from  the  body,   the  anatomical  reason  for  this  conduction 


DILATATION  01*  THE  RIGHT  VENTRICLI]:         337 

at  once  becomes  apparent,  as  weU  as  that  for  the  better  con- 
duction of  the  murmur  to  the  arteries  of  the  left  side  than 
to  those  of  the  right.  The  production  of  a  thrill  is  easy  of 
explanation  by  this  hypothesis,  for  there  is  an  aneurysmal 
dilatation  of  the  pulmonary  artery  into  which  the  blood 
enters  in  a  direction  nearly  at  right  angles  to  the  line  of  the 
artery. 

2.  Accentuation  of  the  Pulmonary  Second  Sound. — 
Accentuation  of  the  pulmonary  second  sound  is  of  course 
of  extremely  common  occm-rence  in  these  cases,  but  is  of  httle 
diagnostic  value  so  far  as  the  presence  or  absence  of  dilatation 
is  concerned.  The  point  of  maximal  intensity  of  the  second 
sound  is  however  of  value  as  giving  an  indication  of  the  situa- 
tion of  the  pulmonary  valves.  Thus  in  dilatation  of  the  right 
ventricle  the  P.M.I,  of  the  second  sound  is  usually  higher 
than  normal,  and  as  the  dilatation  subsides  this  point  may  be 
observed  to  alter  its  position  and  descend  towards  its  normal 
situation. 

The  degree  of  accentuation  of  this  sound  gives  us  also 
important  information  as  to  the  tension  of  the  blood  in  the 
pulmonary  artery,  and  shows  to  some  extent  the  amount  of 
w^ork  wdiich  the  ventricle  is  doing. 

3.  Bruit  de  Diable. — The  venous  hum  usually  associated 
with  anaemia,  which  is  audible  at  the  root  of  the  neck  over 
the  great  veins  and  is  commonly  called  the  bruit  de  diahle,  is 
also  intimately  related  to  failm-e  of  the  right  ventricle,  although 
I  do  not  think  there  are  sufiBcient  reasons  for  tliinking  that 
it  cannot  occur  apart  from  this  failm-e. 

As  is  well  known  this  murmur  is  best  heard  in  the  erect 
position,  and  disappears  to  a  greater  or  less  extent — often 
entnely — when  the  patient  hes  down.  The  pathological  ex- 
planation of  this  is  at  once  made  evident  if  at  a  post-mortem 
on  one  of  these  cases  the  trouble  be  taken  to  distend  the  right 
heart  and  great  veins  with  hard  paraffin  before  its  removal 
from  the  body.  Such  an  injection  shows  very  beautifully 
the  constriction  of  each  dilated  vein  at  the  point  where  it 
joins  another  vein,  due  to  the  mechanical  support  afforded 
at  these  spots.  A  murmur  must  arise  on  the  proximal  side 
of  each  of  these  constrictions  as  the  blood  flows  towards  the 


333  DILATATION  OF  THE  RIGHT  VENTRICLE 

heart  .^  When  the  patient  is  erect  the  action  of  gravitation 
is  to  increase  the  pressure  of  the  blood  liowmg  into  the  innomi- 
nates  and  superior  cava  from  the  head  and  neck,  thus  increasing 
the  distension  of  the  veins.  When  the  patient  is  recumbent 
this  pressure  is  lessened,  and  the  veins  near  the  heart  bemg 
less  distended,  the  relative  constriction  at  the  points  of  junction 
is  less  and  the  venous  hum  lessens  or  disappears  as  a  consequence. 

The  clinical  importance  of  the  venous  hum  is  that  it  shows 
the  existence  of  ^Yant  of  tone  in  the  great  veins.  This  fact 
may  be  of  considerable  importance  if,  as  seems  to  me  probable, 
the  contraction  of  the  veins  plays  an  important  part  not  only 
in  the  fihing  of  the  auricle,  but  also  in  checking  tricuspid 
regurgitation  by  means  of  a  more  prolonged  and  powerful 
contraction  than  normal. 

4.  The  Murmurs  due  to  Tricuspid  Eegurgitation. — 
Theoretical  as  well  as  practical  considerations  seem  to  show 
that  tricuspid  regurgitation  must  accompany  dilatation  of 
the  right  ventricle  (of  the  adult  type) — at  all  events,  if  it  be 
well  marked.  But  from  a  clinical  point  of  view  it  is  sometimes 
difficult  to  point  to  any  physical  sign  w^hich  makes  its  presence 
or  absence  certain  in  any  particular  case.  It  can,  I  think,  be 
truthfully  affirmed  that  there  is  no  phj^sical  sign  which  is 
characteristic  of  tricuspid  regurgitation  in  the  way  in  which 
the  systolic  apical  murmur  with  displacement  of  the  apex 
beat  is  characteristic  of  mitral  regurgitation. 

Perhaps  the  tw^o  most  reliable  signs  are — firstly,  the  presence 
of  a  systoUc  murmur  audible  in  any  or  all  of  the  following 
situations  :  (a)  over  the  body  of  the  right  ventricle,  or  (b) 
over  the  right  auricle,  and  also  (c)  over  the  situation  of  the 
superior  vena  cava  just  to  the  right  of  the  sternum  in  the 
first  and  second  interspaces  ;  and  secondly,  the  presence  of 
true  systolic  pulsation  in  the  veins  of  the  neck  or  over  the  Hver. 

The  diagnostic  value  of  the  former  sign  is  diminished  by 
the  fact  that  it  may  sometimes  be  absent  in  even  w'ell-marked 
cases  of  tricuspid  regurgitation  {vide  p.  280). 

True  pulsation  in  the  veins  of  the  neck  is  almost  absolutely 
reliable  as  a  positive  sign  of  tricuspid  regurgitation,  but  its 

'  The  fact  that  the  murmur  is  slightly  louder  during  diastole  than  during 
systole  is  in  harmony  with  this  theory  of  its  production. 


DILA.TAT10X  OF  THE  RiaHT  VENTRICLE  339 

absence  is  valueless  as  a  negative  sign.  Very  frequently 
cases  of  undoubted  tricuspid  regurgitation  are  met  with 
in  which  this  sign  is  absent.  As  a  most  marked  instance, 
I  may  quote  the  case  of  a  girl  aged  fifteen,  who  was  under 
my  care  in  this  hospital,  suffering  fi'om  mitral  disease,  with 
an  enormously  dilated  heart.  The  apex  was  in  the  axilla 
6|  inches  from  the  sternum.  The  cardiac  pulsation  was 
visible  from  the  second  to  the  seventh  interspaces  inclusive, 
and  extended  to  the  right  of  the  sternum  as  far  as  the  right 
nipple  Ime  (2|  inches).  The  pulsation  to  the  right  of  the 
sternum  was  shown  by  the  cardiograph  to  be  due  to  the 
auricle,  and  there  was  so  much  tricuspid  regurgitation  that 
a  systoHc  thrill  was  clearly  felt  over  the  auricle  in  the 
neighbourhood  of  the  right  nipple  ;  nevertheless,  there  was 
no  venous  pulsation  in  the  neck,  nor  was  there  any  pulsation 
of  the  hver  dming  the  six  months  that  she  was  under 
observation  {vide  p.  404,  Case  V,  and  Plate  XII). 

Systolic  Tricuspid  Murmur. — In  cases  where  there 
is  no  true  pulsation  in  the  veins  of  the  neck  the  tricuspid 
systohc  murmur  is  often  of  great  diagnostic  value.  The 
chief  pomt  of  difficulty  is  its  distinction  from  the  pulmonary 
systolic  murmur.  The  mam  distmguishing  featm-es  are  as 
follow  :  The  area  over  w^hicli  it  is  heard  is,  as  a  rule,  lower  than 
that  of  the  pulmonary  murmur.  The  latter  is  rarely  heard 
below  the  third  space,  whereas  the  area  of  audition  of  a  pm-e 
tricuspid  murmur  is  approximately  an  oval-shaped  area  bounded 
on  the  right  by  the  sternum,  above  by  the  third  rib,  below 
by  the  fifth  rib,  and  extending  a  variable  degree  towards  the 
nipple  line  in  the  fourth  space.  This  area  varies  according 
to  the  amomit  of  dilatation  present,  and  may  be  approximately 
put  do^Tii  as  coinciding  with  the  mner  half  or  two-thirds  of 
the  area  of  the  absolute  dullness. 

A  difference  m  pitch  between  the  two  murmurs  will  some- 
times be  noted  by  which  they  can  be  distinguished,  but  the 
character  of  the  tricuspid  mm-mm-  varies  much  in  different 
cases. 

A  point  of  diagnostic  value  is  sometimes  obtained  in  the  fact 
that  a  tricuspid  regurgitant  mm-mur  is  heard  very  loudly  at 
the  sternal  ends  of  the  second  and  third  right  interspaces 

z  2 


310         DILA.TATION  OF  THE  RIGHT  VENTRICLE 

over  the  situation  which  the  tip  of  the  right  auricular  appendix 
would  occupy  in  a  dilated  heart.  In  my  experience  it  is,  however, 
unusual  to  find  the  murmur  audible  here  in  the  adolescent  type 
of  functional  cases.  It  is  more  common  in  valvular  disease 
and  with  the  adult  type  of  dilatation. 

When  the  murmur  is  audible  in  both  the  first  interspaces 
over  the  great  veins  it  is  very  difficult  to  distinguish  it  from 
an  aortic  murmur.  The  point  to  be  relied  upon  is  its  loudness 
close  to  the  sternum  as  compared  with  its  feebleness  or  absence 
over  the  carotids  and  distal  portions  of  the  subclavians  ; 
a  moderately  loud  aortic  systolic  murmur  being  of  course 
loudly  conducted  along  the  arteries. 

5.  The  Third  Bound  of  the  Heart. — By  this  name 
I  consider  that  we  ought  to  designate  the  sound  which  when 
added  to  the  second  sound  of  the  heart  gives  rise  to  what 
is  known  as  '  a  reduplication  of  the  second  sound  which  is 
audible  only  at  the  apex.'  The  occurrence  of  this  sound  at 
the  apex  or  over  the  right  ventricle  of  the  heart  produces 
one  of  the  varieties  of  what  is  known  as  the  hruit  de  galoj),  or 
triple  sound  of  the  heart.  The  most  familiar  instance  of  its 
occurrence  is  in  mitral  stenosis,  when  there  is  audible  at  the 
apex  a  presystolic  murmur  and  '  reduplicated  second  sound.' 

It  is  of  course  an  abnormal  sound  in  the  human  heart. 
As  regards  the  time  of  its  occurrence,  it  follows  the  second 
sound,  the  interval  being  nearly  equal  to  that  between  the 
first  and  second  sounds,  and,  moreover,  in  any  one  case  the 
interval  appears  to  be  constant  and  does  not  vary  when  the 
heart  is  irregular. 

In  character  it  is  a  faint  sound,  and  is  often,  in  the  cases 
we  are  dealing  with,  inaudible  with  a  wooden  stethoscope 
or  when  the  binaural  stethoscope  is  pressed  too  firmly.  It 
is  very  apt  to  be  inconstant  in  its  occurrence,  and  frequently  is 
only  to  be  heard  with  the  heart  beats  which  occur  during  the 
pause  between  inspiration  and  expiration  and  at  the  com- 
mencement of  expiration.  Its  area  of  audition  is  over  the 
body  of  the  right  ventricle,  and  it  is  not  loud  enough  to  be 
conducted  widely. 

In  the  cases  we  are  now  considering,  clinical  observation 
seems  to  show  that  the  two  factors  upon  which  this  sound  de- 


DILATATION  OF  THE  EIGHT  VENTRICLE         341 

pends  for  its  production  are  the  amount  of  dilatation  of  the  right 
ventricle  and  the  strength  of  the  forces  producing  the  inrush 
of  blood  into  the  ventricle  on  Ihe  opening  of  the  tricuspid 
valve.  Thus  in  a  feebly  acting  and  dilated  ventricle,  wo  get  no 
third  sound,  but  as  the  strength  of  the  heart  increases,  a  third 
sound  often  appears  for  a  time  and  disappears  again  when  the 
ventricle  further  regains  its  tone  and  the  dilatation  disappears. 

I  am  unable  here  to  go  fully  into  the  causation  of  this 
'  third  sound,'  and  I  will  onlj^  say  that  I  feel  sure  that  this 
sound,  as  well  as  the  diastolic  murmur,  which  is  often  closely 
associated  with  it  and  which  will  shortly  be  mentioned,  are  both 
of  them  manifestations  of  an  active  expansion  movement 
on  the  part  of  the  ventricle  whereby  blood  is  sucked  into  it 
from  the  auricle  and  veins  innnediately  after  the  closure  of 
the  semilunar  valves  (;vide  p.  427). 

The  most  marked  instance  of  this  third  sound  and  murmur 
occurs  in  the  left  ventricle  in  mitral  stenosis,  for  there  the  valves 
are  permanently  prevented  from  assuming  their  normal  position 
as  the  ventricle  enlarges  during  its  expansion  movement, 
and  the  ventricle  is,  moreover,  not  only  of  normal  strength, 
but  is  able  also  to  alter  the  mode  and  strength  of  its  contraction 
so  as  to  develop  a  greater  amomit  of  suction,  as  is  evidenced 
by  the  increased  loudness  and  sharpness  of  the  first  sound  in 
mitral  stenosis. 

6.  The  Diastolic  Tricuspid  Murmur. — This  murmur  is 
produced  in  the  same  manner  as  with  the  third  sound  of 
the  heart,  with  which  it  is  so  closely  associated  clinically. 
It  only  remains  to  say  that  the  murmm*  is  usually  faint  and 
low-toned  or  humming,  and  is  audible  simply  over  the  body 
of  the  right  ventricle.  The  outer  limit  of  its  area  of  audition 
is  often  so  sharp  as  to  suggest  the  probability  that  when  present 
the  localisation  of  this  murmur  may  serve  as  a  guide  to  the 
position  of  the  interventricular  septum.  As  regards  its  occur- 
rence, it  is  rare  in  functional  dilatation  in  adolescents,  and 
I  have  only  observed  it  three  or  four  times  out  of  several 
hundred  cases  carefully  examined.  In  dilatation  of  the  right 
ventricle,  secondary  to  valvular  disease,  it  is  much  more 
frequent. 

The  Adult  Type  of  Dilatation. — I  think  I  have  said 


342         DILATATION  OF  THE  RIGHT  VENTEICLE 

enough  already  as  to  the  points  which  separate  the  adolescent 
type,  which  I  have  been  discussing,  from  the  adult  type,  to 
make  further  dwelling  upon  this  subject  unnecessary. 

Dilatation  Secondary  to  Valvular  Disease. — Most  of 
what  I  have  already  said  vnW  be  found  to  apply  to  this  form 
of  dilatation  if  allow^ance  be  made  for  the  effect  of  the  changes 
in  the  left  side  of  the  heart  which  result  from  the  primary 
lesion.  The  main  difference  beween  this  and  the  former 
class  of  case  is  that  the  ventricle  here  is  not  necessarily  weaker 
than  normal,  and  is  of  course  often  hypertrophied.  Speaking 
broadly,  the  dilatation  of  the  heart  to  the  right  of  the  sternum 
is  more  apt  in  these  cases  to  equal  or  exceed  in  amount  that  in 
the  second  and  third  left  interspaces  ;  and  further,  the  systolic 
tricuspid  murmur  is  in  these  cases  more  marked,  and  the 
pulmonary  systolic  murmur  less  likely  to  be  present  than  in 
the  functional  cases.  Other  points  of "  distinction  may  be 
gathered  from  what  I  have  already  said. 

Symptoms.  —  The  symptoms  of  dilatation  of  the  right 
ventricle  are  mostly  of  the  usual  type — namely,  breathlessness, 
palpitation,  Szc.  There  is  one  symptom,  however,  which  is  fairly 
distinctive  of  the  adolescent  type,  and  that  is — pain  localised 
to  the  region  of  the  second  and  third  left  costal  cartilages. 
This  pain  may  be  fairly  acute,  but  more  usually  it  consists 
of  a  dull  pain,  and  is  frequently  accompanied  by  a  sense  of 
tightness  in  this  region  ;  and  there  is  often  in  the  adolescent 
class  of  cases  a  ieeling  as  if  too  large  a  bolus  of  food  had  been 
swallowed  and  was  sticking  in  the  throat  at  the  level  of  the 
second  left  interspace.  These  sensations  are  often  relieved 
somewdiat  wdien  the  patient  takes  a  prolonged  deep  inspiration, 
and  this  sighing  voluntary  inspiration  may  often  be  noted 
in  these  cases.  In  addition,  there  is  sometimes  tenderness 
on  percussion  over  the  dilated  ventricle  in  the  second  left 
interspace,  and  there  may  even  be  tenderness  on  pressure. 

Etiology  of  Dilatation  op  the  Eight  Ventricle. — 
Failure  of  the  right  ventricle  will  result  from  (1)  excessive 
work  thrown  upon  the  normal  ventricle — i.e.  absolute  over- 
strain ;  or  (2)  normal  amount  of  work  thi'own  upon  a  w^eakened 
ventricle — i.e.  relative  overstrain. 

1.  Absolute   Overstrain. — In    this    class    of    case    the 


DILATATION  OF  THE  RIGHT  VENTRICLE  343 

cause  of  the  failure  and  dilatation  of  the  ventricle  is  for  the  most 
part  not  inherent  in  the  ventricle  itself.  The  most  typical 
examples  of  this  class  are  those  in  which  there  is  dilatation  of 
the  right  ventricle  as  a  result  of  overstrain  from  excess  of 
athletic  exercise  or  from  excess  of  heavy  work — such  as  lifting 
heavy  weights — in  otherwise  strong  and  healthy  young  men. 
These  oases  may  be  subdivided  into — {a)  those  in  which  the  strain 
upon  the  right  ventricle  is  indirect  and  due  to  the  demands  of 
the  systemic  circulation,  as  is  the  cases  above  mentioned,  or 
in  valvular  disease  of  the  heart ;  or  (b)  those  in  which  the  strain 
is  due  to  primary  embarrassment  of  the  pulmonary  circulation. 
Of  this  the  most  typical  instance  is  of  course  emphysema. 
Pneumonia  also  produces  dilatation  from  this  cause,  and  I 
believe  that  we  must  also  include  in  this  category  many,  if 
not  most,  of  the  common  cases  of  dilatation  of  the  right  ventricle 
in  anaemia  and  chlorosis.  Of  course,  in  these  last-named 
cases,  a  prominent  feature  is  the  weakness  from  the  anaemic 
state  of  the  blood  ;  but  I  think  we  have  sufficient  ground  for 
believing  that  there  is  in  addition  an  abnormal  amount  of  con- 
traction of  the  pulmonary  arterioles  (or  venules)  caused  by  the 
poor  state  of  the  blood.  This  is  a  subject  for  physiological 
experiment.  The  fact  that  in  suffocation  there  is  a  spasm 
of  the  pulmonary  arterioles  which  is  removed  by  m'trite  of 
amyl,  as  has  recently  been  pointed  out  bj^  Sir  George  Johnson, 
is  in  favour  of  the  above  supposition.  Two  years  ago,  in  my 
thesis  for  the  degree  of  M.D.,  I  expressed  my  belief  that  the 
pulmonary  vasomotor  system  had  in  all  probability  much  to 
do  with  the  failure  of  the  right  side  in  anaemia  ;  but  unfortu- 
nately ill-health  has  prevented  me  from  investigating  this 
subject  further,  except  so  far  as  to  enable  me  to  say  that  there 
seems  every  probability  that  nitrites  may  prove  of  considerable 
value  in  these  cases. 

2.  Eelative  Overstrain  as  a  Cause  of  Dilatation  of 
THE  Eight  Ventricle. — As  a  typical  instance  of  this,  I  may 
give  the  dilatation  which  is  apt  to  occm*  after  the  fall  of  the 
temperature  in  rheumatic  fever,  but  more  especially  when 
the  patient  first  begins  to  get  up.  In  such  a  case,  I  have 
seen  the  right  ventricle  dilate  out  nearly  to  the  left  nipple  line 
in  the  second  left  interspace  in  the  course  of  a  day  or  two. 


344         DILATATION  OF  THE  RIGHT  VENTRICLE 

The  dilatation  in  cases  of  anaemia  and  chlorosis  is  also 
in  part  due  to  weakening  of  the  ventricle  from  malnutrition  ; 
and,  as  another  instance,  may  be  mentioned  the  weakening 
due  to  many  acute  febrile  conditions. 

In  conclusion,  I  may  say  that  we  have  much  yet  to  learn 
as  to  these  changes  in  the  right  side  of  the  heart,  and  that  there 
is  scope  for  much  careful  clinical  study  as  to  the  effect  of  drugs 
upon  the  pulmonary  circulation,  upon  the  great  veins,  and 
upon  the  character  and  strength  of  the  important  expansion 
movement  of  the  ventricle. 


Essay  VIII.— ON  DISPLACEMENT  OF  THE  HEART 

This  essay  will  be  chiefly  devoted  to  those  kinds  of  displace- 
ment which  are  of  both  interest  and  importance  to  the 
clinician,  and  it  is  not  intended  to  take  up  cases  where  the 
interest  in  mainly  anatomical,  such  as  the  changes  which  take 
place  in  the  situation  of  the  heart  and  the  relative  position  of 
its  chambers  in  spinal  curvature.  Moreover,  as  this  essay 
is  based  entirely  upon  observations  by  the  bedside,  the  question 
as  to  the  amount  and  the  degree  of  rotation  of  the  heart  upon 
itself  which  results  from  lateral  displacement  of  the  organ  is 
scarcely  touched  upon. 

Clinically,  all  cases  of  cardiac  displacement  may  be  divided 
into  two  main  groups  : — 

Firstly,  those  where  the  position  of  the  heart  in  the  thorax 
is  altered  as  a  result  of  a  change  in  the  heart  itself  or  its 
great  vessels  (e.g.  by  aneurysm).  In  this  case  the  cause  of 
displacement  may  be  said  to  be  intrinsic. 

Secondly,  where  some  extrinsic  cause  of  displacement  is 
at  work  and  the  position  of  the  heart  is  altered  as  a  result 
of  changes  in  the  surrounding  viscera  (e.g.  displacement  of  the 
heart  by  a  pleural  effusion). 

I.  Caediac  Displacement  due  to  Changes  within   the 
Heart  Itself 

Amongst  the  intrinsic  causes  of  displacement  of  the  heart, 
a  common  one  is  that  due  to  aneurysm.  As  regards  the 
displacement  due  to  aneurysm  of  the  aorta  arising  outside  the 
pericardium  no  serviceable  generalisation  can  be  made,  for 
the  amount  and  type  of  displacement  depends  upon  the  size 
of  the  aneurysm  and  the  situation  where  it  develops. 

In  the  case  of  intra-pericardial  aneurysm  arising  in  or  near 

345 


346  DISPLACEMENT  OF  THE  HEART 

the  anterior  sinus  of  Valsalva,  a  characteristic  displacement 
seems  to  result — although  the  writer's  experience  has  been 
too  hmited  tamake  a  certain  generahsation. 

An  aneurysm  arising  in  this  situation  se.ems  to  displace 
the  right  auricle  downwards  and  to  the  right,  and  the  right 
ventricle  outwards  to  the  left  and  downwards.  Such  a  dis- 
placement is  shown  in  the  accompanying  figure — drawn  from 
a  photograph  taken  at  the  post-mortem  examination  of  a  case 

of    intra-pericardial    anemysm 
{vide  fig.  128). 

Closely  alhed  to  the  dis- 
placement of  the  heart  due  to 
aneurysm  is  that  noticeable  in 

^/2eM/7-s/w/-J^/^^;^^f5^o^'"'3c?^ZA^  ]       cases  of  aortic  regurgitation. 

In  many  text-books  the  fact 
^'S'M -lA^^^^^'^^l^'^^'^^W        is  noted  that  the  apex  of  the 

heart  m  weli-marked  aortic 
regurgitation  lies  at  a  relatively 
lower  level  than  is  the  case 
when  the  enlargement  is  due 
to  mitral  regurgitation,  and  it 
is  stated  that  whereas  in  the 
Pjq  J28  latter  the   apex   of  the   heart 

Situation  of  heart  showing  downward  llGS  HI  Or  external  tO  the 
displacement  duo  to  intra-pericardial  aneurysm,  oricrinal  axis  of  tllP  heart  in 
(ilade  from  a  photograph.)  o  _  ' 

aortic  regurgitation,  on  the 
other  hand,  the  apex  is  apt  to  be  internal  to  the  original 
axis — i.e.  hes  at  a  relatively  lower  level  than  in  mitral 
regurgitation.  Various  reasons  for  this  are  given,  but  I 
have  not  yet  come  across  the  following,  which  seems  the  true 
explanation. 

In  such  cases  as  these  it  can,  as  a  rule,  be  easily  recognised 
that  the  point  of  maximal  loudness  of  the  pulmonary  second 
sound,  as  well  as  the  upper  border  of  the  cardiac  dullness, 
are  both  lower  than  normal,  and  therefore  it  is  justifiable  to 
state  that  the  lowering  of  the  apex  beat  is  in  all  probability 
due  to  a  displacement  downwards  of  the  whole  heart  rather 
than  simply  to  a  special  downward  increase  of  the  left 
ventricle  alone. 


DISPLACEMENT  OF  THE  HEART  347 

The  explanation  of  this  downward  displacement  is  to  be 
found  in  the  fact  that  over-distension  of  the  first  part  of  the 
aorta  is  a  necessary  consequence  of  the  establishment  of 
compensation  in  Avell-marked  aortic  regm-gitation. 

The  reason  for  this  may  be  given  shortly  as  follows  : — 

It  may  be  taken  for  granted  that,  when  the  muscular  power 
of  the  heart  is  good,  a  definite  amount  of  blood  (approximately 
3  ounces)  ought  to  pass  into  the  arteries  at  each  contraction 
of  the  ventricle. 

In  order  to  bring  this  about,  when  there  is  leakage  of  some 
of  the  blood  back  through  the  aortic  valves  at  each  beat,  it 
is  necessary  for  the  ventricle  to  throw  forward  with  each 
contraction  an  extra  amount  of  blood  in  order  to  allow  for 
the  leakage.  This  extra  amount  must  be  at  least  equal  to 
the  normal  amount  plus  the  amount  of  the  leakage.  There- 
fore, if  at  each  beat  half  an  ounce  leak  back,  the  ventricle  must 
throw  rather  more  than  3|  ounces  into  the  aorta  at  each 
contraction  if  '  compensation  '  is  to  be  established.  In  other 
words,  the  process  of  compensation  in  aortic  regurgitation 
demands  that  an  amount  of  blood  considerably  above  the  normal 
must  be  thrown  into  the  aorta  at  each  beat,  and  it  must 
therefore  be  abnormally  distended  by  the  ventricular  systole. 

Now,  as  fluid  pressure  acts  equally  in  all  directions,  this 
distensile  force  will  not  only  tend  to  produce  the  well-known 
increase  in  the  transverse  diameter  of  the  aorta,  but  also  to 
stretch  it  longitudinally  as  w-ell,  and  the  lengthening  of  the 
aorta  which  must  be  thus  brought  about  must  tend  to  displace 
the  heart  downwards.  I  have  no  doubt  that  careful  measure- 
ments of  the  level  of  the  aortic  valves  post-mortem  in  a  series 
of  cases  of  aortic  regurgitation  would  prove  definitely  that  this 
is  so. 

Owing,  however,  to  the  elasticity  of  the  aorta  it  is  not 
likely  that  this  downward  displacement  of  the  heart  would 
be  as  evident  after  death — when  the  distensible  force  of  the 
blood  pressure  is  no  longer  acting — as  it  is  during  life. 

Of  all  the" 'intrinsic  causes  of  alteration  in  the  position  of 
the  heart,  by  far  the  commonest  is  the  upward  displacement 
of  the  apex  which  occurs  in  anaemia. 

The  late  Dr.  Foxwell  was,  I  believe,  the  fiist  to  point  out 


348  DISPLACEMENT  OF  THE  HEART 

the  frequency  of    this  phenomenon  and    its  probable  cause 
{vide  his  '  Essays  in  Heart  and  Lung  Disease,'  p.  343). 

The  subject  of  upward  displacement  is  discussed  at  length 
in  the  following  pages. 

Upward  Displacement  of  the  Heart  by  Intrinsic 
Causes 

The  intrinsic  causes  of  elevation  of  the  apex  are  of  con- 
siderable interest  and  importance  chnically.  In  the  first 
place,  dilatation  of  the  right  ventricle  downwards  may,  under 
certain  circumstances,  cause  a  recognisable  degree  of  elevation 
of  the  apex.  Since  the  right  ventricle  occupies  the  inferior 
aspect  of  the  heart  and  rests  upon  the  diaphragm,  any  abnormal 
fullness  of  this  chamber  must,  theoretically,  raise  the  apex  of 
the  heart  to  some  extent ;  but  this  rise,  due  to  right  ventricular 
dilatation,  would  not  be  recognisable  clinically,  being  so  small. 
When,  however,  the  heart's  fixation  to  the  diaphragm  by  the  in- 
ferior vena  cava  is  taken  into  account  it  will  be  seen  that,  taking 
this  point  as  the  fulcrum  of  a  lever,  the  effect  of  a  bulging  of 
the  right  ventricle  at  a  spot  near  the  fulcrum  will  cause  a  much 
greater  effect  at  the  cardiac  apex,  which  hes  at  a  considerable 
distance  from  the  fulcrum.  If  the  point  where  the  dilated 
right  ventricle  presses  on  the  diaphragm  lies,  say,  2  inches  away 
from  the  fixation  point  (inferior  vena  cava),  and  the  apex  lies 
6  inches  away,  any  downward  dilatation  of  the  ventricle 
would  give  a  threefold  effect  at  its  apex,  and  an  increase  of 
I  inch  in  the  right  ventricle  (supposing  the  diaphragm  to  be 
unyielding)  would  give  a  |  inch  rise  of  the  apex. 

As  the  structures  concerned  are  not  rigid,  but  elastic,  it  is 
not  easy  to  say  how  far  the  mechanical  principles  just  enun- 
ciated will  apply :  but  occasionally  a  case  is  met  with  where 
the  upward  displacement  of  the  apex  appears  to  he,  due  to 
the  cause  here  suggested. 

Another  intrinsic  cause  of  elevation  of  the  apex  is  found 
in  the  changes  which  take  place  in  the  heart  when  it  fails  and 
dilates  as  a  result  of  ansemia  in  adolescence,  and  this  cause 
of  elevation  of  the  apex  is  of  considerable  clinical  interest 
and  importance. 

Although  the  fact  of  the  elevation  of  the  apex  is  clearly 
demonstrated  by  clinical  observation,  the  explanation  of  the 


UPWAKD  DISPLACEMENT  OF  APEX 


349 


mechanism  whereby  it  is  brought  about  is  neither  clear  nor  easy 
of  explanation,  although  it  certainly  seems  due  to  changes 
■within  the  heart  itself. 

The  chnical  facts  upon  which  any  theory  must  be  based 
are  these  : — 

1.  In  anaemic  dilatation  of  the  right  ventricle — such  as  is 
seen  in  adolescents — the  apex  is  frequently  raised  above  the 
normal  level.  The  careful  study  of  192  patients  with  w'ell- 
marked  dilatation  showed  that  the  apex  was  raised  above  the 
level  of  the  fifth  interspace  in  87  out  of  192  observations,  and 
normal  in  105 — i.e.  it  was  distinctly  raised  above  the  normal 
level  in  45'3  per  cent,  of  the  cases. 

2.  As  regards  age  as  a  factor  in  this  rise.  In  the  first 
place,  Is  the  apex  more  displaced  in  more  distensible  or  in  less 
distensible  hearts  ?  To  try  to  answer  this  question,  I  have 
tested  the  relationship  which  the  age  of  the  patient  bears  to 
the  presence  or  absence  of  upward  displacement  of  the  apex. 
It  was  more  frequent  in  patients  between  twenty  and  twenty- 
five  years  of  age  than  in  younger  patients ;  for  58  per  cent,  of 
the  former  and  less  than  40  per  cent,  of  the  latter  had  a  raised 
cardiac  apex. 

The  figures  available  are  as  follows  : — 


Age 

No.  of  cases 

With  raised  apes 

With  normal  apei 

13  to  19 
20  to  25 

103 
75 

178 

41(=39-8%)       1       62(=60-2o/„) 
44  (=  58-6%)       1       31  (=  41-4%) 

85                                    93 

The  foUomng  are  more  detailed  figures  :— 

- 

Ase 

No.  of  cases    !        Witii  raised  apex 

With  normal  apex 

^r                  1  13  to  15 

Younger   L  g  to  18 
group   1        jg 

Older        j  20  to  21 
group    \  22  to  25 

12 
59 
32 

103 

42 
33 

75 

6                                   6 
22  {=31%)         '      37(=G3%) 
13  (=  40%)              19  (=  60%) 

41  (=  39-8%)      j      62  (=  60-2%) 

27  (=  64-2%)           15  (-  35-8%) 
17  (=51-5%)           16  (=48-5%) 

44  (=  58-6%)           31  {=  41-4%; 

350 


DISPLACEMENT  OF  THE  HEART 


Again,  the  fact  that  a  raised  apex-beat  is  more  hkely  to 
be  foimd  in  an  older  than  a  younger  adolescent  with  anaemia 
is  shown  by  an  analysis  of  the  whole  of  the  85  cases  with  a 
raised  apex-beat.  Fifty-seven  of  them,  or  67  per  cent.,  were 
nineteen  years  of  age  or  more,  and  only  33  per  cent,  were  mider 
nineteen,  whereas  in  the  group  with  normal  apex  54  per  cent, 
only  were  in  the  older  group  and  46  in  the  yoimger. 

But  age  as  an  etiological  factor  ought  also  to  be  studied 
in  relation  to  the  amomit  of  the  right  ventricular  dilatation 
present  in  the  cases.  For  this  purpose,  I  here  give  the  average 
amount  of  relative  cardiac  dullness  wliich  was  detected  in 
the  second  left  interspace  when  the  breath  was  held  in 
expiration. 

In  this  connection,  I  have  eliminated  those  cases  where  there 
was  no  marked  dilatation  of  the  heart  upwards,  because  in 
none  of  these  was  the  apex  above  the  normal  level- 
In  this  way  the  available  cases  are  reduced  to  114. 
I  have  divided  them  into  four  groups — namely,  those  four- 
teen to  fifteen  years  of  age,  those  sixteen  to  eighteen,  nineteen 
to  twenty-one,  and  twenty-two  to  twenty-five  respectively; 
and  the  subjoined  table  shows  the  number  of  cases  in  each 
group  in  which  the  apex  was  raised  above  the  lifth  interspace 
and  also  the  average  amount  of  relative  cardiac  dullness  in 
the  second  left  interspace  in  each  group. 


Age 

No.  of  cases 

No.  with  apex 
in  fourth  space 

No.  with  apex 
in  fifth  space 

Average  amount  of  dila- 
tation in  second  space    j 

14  to  15 
16  to  18 
19  to  21 
22  to  25 

7 
40 
48 
19 

114 

3 
11 
27 
11 

52 

4 
29 
21 

8 

62 

1 
1*2  iucli. 
1-07   „ 
1-37  „ 
11     „ 

Average  dilatation 
1-2  inch 

These  results  seem  to  show  that  in  patients  over  twenty- 
one  years  of  age  there  is  a  greater  tendency  for  the  apex  to 
be  displaced  upwards  when  there  is  only  a  moderate  degree 
of  upward  dilatation  than  there  is  in  the  younger  patients. 

In  the  case  of  those  aged  nineteen,  twenty,  and  twenty-one, 


UPWAKD  DISPLACEMENT  OF  APEX 


351 


a  reliable  comparison  is  not  possible,  owing  to  the  greater 
amount  of  upward  dilatation  which  occurred  in  them. 

The  question  of  the  bearing  of  the  age  of  the  patient  upon 
the  displacement  of  the  apex  may  be  studied  in  another  way 
—namely,  by  dividing  up  the  cases  into  groups  according  to 
the  amount  of  upward  dilatation  present,  and  then  notin^ 
the  relative  ages  of  the  patients,  showing  upward  displacement 
of  the  apex,  as  compared  with  those  whoso  apex  beat  was 
in  the  normal  situation. 

The  results  are  as  follows  : — 


Total 
Amount  o£       number 
dilatation             of 

cases 

Average 
age  of 
group 

No.  of 
cases  with 
apex  in 
foiurth 
space 

Per 
cent. 

Average 
age 

Cases 

with 

normal 

apex 

Average 
age 

1  inch  or  less 
Over  1  inch 
Dilatation  in 

third  space 

only 

67 
55 
24 

146 

19-4  yrs. 
18-9  yrs. 
20-6  yrs. 

26 
32 

8 

66 

38-8 
58-1 
33-3 

19-8  yrs. 
19-3  yrs. 
22-5  yrs. 

41 
23 
16 

80 

19-3  yrs. 
18-1  yrs. 
19-7  yrs. 

These  tables  show  clearly  that  the  age  of  the  patient  is 
an  important  factor  in  determining  wdiether  the  apex  will  be 
raised  or  not  in  a  case  of  upward  dilatation  of  the  right  ventricle. 
Thus,  in  a  group  of  55  patients  who  show^ed  more  than  1  inch 
of  relative  cardiac  dullness  in  the  second  left  interspace  and 
whose  average  age  was  18*9,  the  average  age  of  the  32  patients 
who  showed  a  raised  apex  beat  was  19-3  years,  whereas  that 
of  the  23  patients  who  had  a  normal  apex  beat,  was  only  18-1 
years . 

In  the  group  of  patients  with  1  inch  or  less,  the  ages  of  those 
with  raised  apex  and  normal  apex  are  practically  the  same — 
namely,  19*8  years  and  19-3  years  respectively. 

In  the  last  group  with  wdiich  the  table  deals — ^namely,  those 
showing  no  dilatation  in  the  second  left  interspace,  but  some 
dilatation  in  the  third,  the  greater  age  of  the  patients  with  a 
raised  apex  beat  is  very  marked  ;  but  as  the  group  is  only  a 
small  one  too  much  stress  cannot  be  laid  on  the  results. 

They  are,  however,  striking — namely,  the  eight  cases  with 


352  DISPLACEMENT  OF  THE  HEART 

upward  displacement  of  the  apex  averaged  2'2-5  years  of  age 
and  the  sixteen  with  normal  apex  averaged  only  19* 7. 

These  facts  seem  to  suggest  that  the  displacement  of 
the  apex  is  associated  with  a  stretching  of  the  wliole  anterior 
wall  of  the  ventricle ;  for  this  type  of  stretching  is  more  likely 
to  occur  in  the  less  distensible  hearts  of  girls  of  twenty  rather 
than  in  the  more  distensible  hearts  of  younger  girls,  for  in 
them  the  upper  part  of  the  anterior  wall  only  is  the  most 
apt  to  dilate. 

1.  Amount  of  Upward  Dilatation  as  a  Factor  in  causing 

Upward  Displacement  of  the  Apex 

The  table  just  given  shows  clearly  that  the  apex  is,  ceteris 
paribus,  more  apt  to  be  displaced  in  cases  showing  much 
dilatation  than  in  those  showing  little  dilatation.  Thus  out 
of  67  cases,  where  there  was  1  inch  or  less  of  dilatation,  the 
apex  was  displaced  up  in  26 — i.e.  in  38*8  per  cent. ;  Avhereas  out 
of  55  cases  showing  more  than  1  inch  of  relative  dullness  the 
apex  was  displaced  up  in  32  cases,  or  58'1  per  cent. 

Therefore,  there  seems  to  be  a  direct  relationship  between 
the  amount  of  dilatation  in  the  second  left  interspace  and 
the  liability  of  the  apex  to  be  displaced  upwards.  It  must, 
however,  not  be  forgotten  that  this  is  only  one  factor,  and  that 
great  upward  dilatation  of  the  right  ventricle  can  exist  without 
a  ly  upward  displacement  of  the  apex. 

2.  Broadening   of   the    Cardiac   Dullness   to   the   Left 

AS  A  Factor    in   causing    Upward   Displacement   of 
the  Apex 

In  certain  cases,  as  already  pointed  out,  the  right  ventricle 
dilates  outwards  to  the  left,  causing  an  abnormal  broadening 
of  the  cardiac  dullness  in  the  third  left  interspace,  which  may 
or  may  not  be  accompanied  by  an  extension  of  the  right 
ventricle  upwards  into  the  second  interspace. 

We  have  seen  in  the  last  table  that  where  this  type  of 
dilatation  occurs  the  apex  was  elevated  in  five  out  of  fourteen 
cases  namely — 35*7  per  cent.  ;  but  it  will  be  interesting  to  see 
whether  upward  displacement  of  the  apex  is  more  frequent 


UPWARD  DISPLACEMENT  OF  APEX  353 

where  this  type  of  dilatation  accompanies  the  upward  distension 
of  the  ventricle  than  where  it  does  not. 

For  the  purposes  of  this  inquiry,  the  available  cases  are 
reduced  to  forty-three,  because  all  those  in  which  there  was  more 
than  1  inch  of  relative  dullness  in  the  second  left  interspace 
have  broadening  of  the  cardiac  dullness  in  the  third  interspace 
and  are  therefore  useless  for  comparison.  Other  cases  are  not 
available,  owing  to  absence  of  any  note  as  to  the  amount  of 
dullness  in  the  third  left  interspace. 

Of  the  43  cases  where  there  was  1  inch  or  less  of  relative  dull- 
ness in  the  second  interspace  26  showed  dilatation  in  the  third 
interspace  and  20  showed  a  normal  amount  of  cardiac  dullness. 

Of  the  26  with  dilatation  in  the  third  interspace  the  apex 
was  displaced  upwards  in  14,  or  more  than  half,  and  normal 
in  12  out  of  the  26  ;  whereas  out  of  those  with  normal 
dullness  in  the  third  interspace  there  was  upward  displace- 
ment of  the  apex  in  only  7  out  of  20  cases,  or  about  one- 
third,  showing  as  before  that  an  increase  of  the  cardiac 
dullness  to  the  left  is  more  apt  to  accompany  elevation  of  the 
apex  than  is  the  case  with  upward  dilatation. 

Further  evidence  as  to  the  causal  relationship  between 
the  dilatation  of  the  right  ventricle  and  the  displacement 
upwards  of  the  apex  is  furnished  by  the  fact  that  out  of  the 
220  cases  of  heart  failure  in  anaemia  there  were  only  two 
in  which  the  apex  of  the  heart  was  raised  above  the  normal 
position  in  the  absence  of  dilatation  of  the  ventricle  upwards 
and  to  the  left. 

Once,  in  the  case  of  a  patient  aged  twenty-four,  with  some 
tricuspid  regurgitation,  where  an  um-ecognised  downward 
enlargement  of  the  right  side  of  the  heart  might  have  lifted 
the  apex  {vide  p.  237),  and  once  in  the  case  of  a  patient  whose 
physical  signs  were  anomalous  m  other  ways,  there  was  a  well- 
marked  systolic  pulmonary  murmur,  but  no  upward  or  outward 
dilatation  of  the  right  ventricle,  and  the  murmur  was,  moreover, 
louder  in  the  erect  than  in  the  recumbent  attitude.  For 
the  further  discussion  of  this  case,  vide  p.  274. 

There  is  another  possible  factor  at  work  in  the  upward 
displacement  of  the   apex  in   these   cases   of  ansemic  heart 

2   A 


354  DISPLACEMENT  OF  THE  HEAKT 

failure,  but  I  am  not  able  at  present  to  speak  definitely  for 
or  against  its  impoitance.  I  refer  to  a  possible  diminution  in 
the  size  of  the  left  ventricle  as  a  contributory  factor  towards 
the  raising  of  the  apex. 

As  has  been  pointed  out  (p.  243),  there  is  distinct  evidence 
of  a  hindrance  to  the  passage  of  the  blood  through  the  lungs 
in  many  cases  of  anaemia,  and  it  may  be  that  this,  coupled 
with  the  weakness  of  the  right  heart,  may  lead  to  a  lessened 
supply  of  blood  to  the  left  side  and  a  consequent  diminution 
in  its  size. 

Careful  study  of  the  size  of  the  liver  and  the  level  of  the 
diaphragm  throughout  a  series  of  cases  would  tend  to  clear 
up  this  point. 

3.  Dilatation  to  the  Eight  not  a  Factor   in   thej 
Causation  of  a  Eaised  Apex 

A  rise  in  the  level  of  the  apex  of  the  heart  is  not  as  a  rule 
associated  with  dilatation  of  the  right  ventricle  to  the  right  of 
the  sternum,  and  this  type  of  dilatation  does  not  play  any 
part  in  the  causation  of  the  apex  rise.  It  is  in  fact  less 
frequent  among  cases  with  a  raised  apex-beat  than  among 
those  with  the  apex  at  a  normal  level. 

The  figures  are  as  follows  : — 

Taking  as  normal,  cases  where  there  was  |  inch  of  relative 
dullness  to  be  detected  to  the  right  of  the  sternum  on  full 
expiration,  and  as  abnormal  those  cases  which  showed  more, 
the  following  facts  are  obtained  :  Out  of  the  85  cases  with  a 
raised  apex  beat  there  were  only  5  wliich  showed  an  abnormal 
amount  of  cardiac  dullness  to  the  right  of  the  sternum — that  is, 
5*8  per  cent.  Whereas  among  the  93  cases  with  the  apex  at 
a  normal  level  there  were  10  with  dilatation  to  the  right,  or 
10"7  per  cent. 

If  the  cases  with  a  raised  apex  be  further  analysed  it  will 
be  found  that  those  showing  dilatation  are  more  numerous 
among  the  older  cases  of  anaemia.  In  those  of  eighteen  or  under 
(28  in  number),  there  was  only  one  case  of  dilatation  of  the 
heart  to  the  right ;  whereas  among  the  57  cases  nineteen  years 
of  age  or  more  there  were  4  cases  of  dilatation,  or  7  per  cent. 

Among  the  cases  with  the  apex  at  a  normal  level  4  out  of  the 


UPWAED  DISPLACEMENT  OF  APEX 


;j&o 


43  patients  who  were  eighteen  or  less  had  some  dilatation — 
i.e.  9'3  per  cent.  ;  and  out  of  the  60  in  the  older  group,  G,  or  10 
per  cent.,  had  some  dilatation.  Therefore,  these  figures  show 
that  dilatation  to  the  right  is  less  frequent  when  the  apex  is 
raised  than  when  it  is  at  a  normal  level,  and  they  also  show 
clearly  the  extreme  infrequence  of  dilatation  to  the  right  in 
those  cases  of  cardiac  failure  due  to  ansemia  in  young  patients. 
For  in  the  cases  with  a  raised  apex  the  right  border  of  the 
heart  was  normal  in  94'2  per  cent,  and  in  those  with  a  normal 
apex  it  was  normal  in  89*3  per  cent. 

4.  Tricuspid  Eegurgitation  not  associated  with  a 
Eaised  Apex 

As  regards  the  presence  of  a  tricuspid  muimur  in  cases 
with  a  raised  apex  beat  it  can  also  be  said  that  the  changes 
in  the  heart  which  produce  this  murmur  do  not  act  as 
factors  in  the  causation  of  the  upward  displacement  of 
the  apex. 

Amongst  the  178  cases,  there  was  a  systohc  murmui-  present 
in  41  instances,  or  23  per  cent.,  and  of  these  the  murmur  is  noted 
as  being  faint  in  12  instances.  The  cases  with  tricuspid  mur- 
mur are  fairly  equally  divided  between  those  with  an  upwardly 
displaced  and  those  with  a  normal  apex  beat — namely,  21  among 
the  former  and  20  among  the  latter ;  giving  a  greater  frequency 
among  those  %vith  a  raised  apex — i.e.  24'7  per  cent,  as  against 
21*5  per  cent.  If,  however,  only  cases  with  a  well-marked 
murmur  be  considered,  the  frequency  of  occm-rence  of  such  a 
murmur  is  the  same  in  both  classes — i.e.  16*4  per  cent,  in  those 
with  a  raised  apex  and  16"1  per  cent,  in  those  with  the  apex 
beat  at  the  normal  level. 

It  is  among  the  younger  patients  with  raised  apex  that  the 
gi-eater  frequency  of  a  faint  tricuspid  mm-mur  occm-s.  For  if  the 
cases  who  are  over  eighteen  alone  be  compared,  it  is  found  that 
out  of  the  57  cases  with  an  upward  displacement  of  the  apex 
there  was  a  tricuspid  murmur  (well  marked  or  faint)  in  28-1  per 
cent,  and  among  those  with  a  normal  apex  beat  in  28  per  cent, 
of  the  cases. 

Therefore,  it  is  clear  that  there  can  be  no  causal  relation- 
ship between  the  agencies  producing  the  upward  displacement 
of  the  apex  and  those  causing  the  appearance  of  a  systolic 
tricuspid  murmur. 

2rA  2 


356 


DISPLACEMENT  OF  THE  HEART 


5.  Failure  of  Left  Ventricle  not  associated  with 
A  Eaised  Apex 

The  evidence  all  -points  to  the  fact  that  failure  of  the 
left  ventricle  does  not  play  any  part  in  causing  the  rise 
of  the  apex  beat,  for  it  is  on  the  whole  less  frequent  in  these 
cases  than  in  those  with  a  normal  apex  beat. 

As  evidence  on  this  point  it  is  not  possible  to  take  out- 
ward displacement  of  the  apex  as  a  sign  of  failure  of  the  left 
ventricle  because  the  rotation  of  the  heart  which  carries  the 
apex  up  into  the  fom-th  interspace  must  at  the  same  time 
swing  it  outwards  external  to  the  nipple  line. 

Evidence  can  only  be  sought  therefore  from  noting  the 
frequency  of  a  mitral  systolic  murmur  in  the  two  gi'oups  of, 
cases. 

The  figures  are  as  follows  : — 

Among  the  178  cases  dealt  with,  a  systolic  mitral  murmur  was 
found  to  be  present  38  times — i.e.  in  21  per  cent.  ;  but  of  these 
it  was  only  a  faint  murmur  in  12  instances,  thus  there  was  a 
well-marked  mm-mur  in  only  26,  or  14*6  per  cent,  of  the  total 
number  of  cases. 

Among  the  85  cases  with  a  raised  apex  beat,  a  mitral  systolic 
murmur  was  present  in  16  instances,  or  18'8  per  cent.,  and 
was  well  marked  in  only  12*9  per  cent.  ;  whereas  among  the  93 
with  a  normal  apex  a  murmur  was  present  in  22,  or  23*6  per 
cent.,  and  well  marked  in  15,  or  16  per  cent. 

The  detailed  figures  are  as  follows  : — 


With  raised  apex 

With  normal  apex 

No. 

Mitral  murmur 

No. 

Mitral  murmur 

Age  18  or  under  . 

Age  19  or  over    . 

28 
57 

•^  —      '  /o 
14  =  24-5% 

43 

50 

9  =  20-9% 
13  =  26% 

85 

16  =  18-8% 

93 

22  =  23-6% 

With   well-marked 
murmur 

— 

11  =  12-9% 

— 

15  =  16% 

It  can  therefore  be  said  that  failure  of  the  left  ventricle 
is  not  only  7iot  a  factor  in  the  causation  of  an  upward  dis- 


UPWARD  DISPLACEMENT  OF  APEX  357 

placement  of  the  apex  iii  the  cases  we  are  cleaUng  with,  but 
that  its  presence  seems  to  render  the  occurrence  of  upward 
displacement  less  liable  to  occur. 

Conclusions  as  to  the  Cause,  of  Upward  Displacement 
OF  THE  Apex 

Having  now  summarised  the  facts  which  the  study  of 
the  178  cases  of  anaemia  has  elicited,  we  are  in  a  position 
to  discuss  the  cause  of  the  upward  displacement  of  the  apex. 

Firstly,  it  is  rather  more  frequent  in  older  than  in  younger 
adolescents.  Now,  as  has  already  been  pointed  out,  in  the 
yomiger  patients,  the  dilatation  of  the  right  ventricle  is  more 
apt  to  be  hmited  to  the  thin  anterior  part  of  the  muscular  wall 
near  the  pulmonary  valves  ;  whereas  in  older  adolescents 
(owing  presumably  to  the  increasmg  strength  of  the  fibrous 
tissues  of  the  heart),  there  is  more  tendency  of  the  ventricle 
wall  to  give  way  evenly. 

1.  Therefore,  it  can  be  asserted  that  the  general  yielding 
of  the  wall  of  the  ventricle  does  appear  to  play  some  part  in 
the  causation  of  the  rise  of  the  apex  beat,  whereas  the  yielding 
of  the  so-called  conus  arteriosus,  apart  from  general  dilatation 
of  the  ventricle,  does  not. 

2.  Where  the  general  dilatation  of  the  ventricle  is  so 
marked  that  the  right  border  of  the  heart  is  carried  beyond 
its  normal  position,  the  apex  beat  is  less  hkely  to  be  found 
raised  above  its  normal  level  than  is  the  case  where  the  right 
border  of  the  heart  is  normal. 

3.  Upward  displacement  of  the  apex  is  less  likely  to  occur 
where  the  left  ventricle  is  becoming  dilated  than  it  is  in  those 
cases  where  the  left  side  of  the  heart  shows  no  signs  of  dilation. 

Therefore,  the  conditions  which  tend  to  favour  a  rise  of 
the  apex  beat  appear  to  be  a  general  dilatation  of  the  anterior 
wall  of  the  right  ventricle  combined  with  a  normal  right  border 
of  the  heart  and  a  left  ventricle,  which  does  not  show  any 
signs  of  enlargement. 

A  consideration  of  the  physical  conditions  which  these 
three  factors  bring  about  suggests  that  the  main  factor  in  the 
causation  of  the  rise  of  the  apex  beat  is  such  an  extension  of 


358  DISPLACEMENT  OF  THE  HEART 

the  right  ventricle  towards  the  left  as  to  carry  the  anterior 
margin  of  the  interventricular  septum  to  the  left  of  its 
normal  situation. 

We  may  therefore  say  that  the  apex  is  rotated  up  in  those 
cases  where  there  is  a  tendency  to  dilatation  of  the  main 
cavity  of  the  right  ventricle  without  any  yielding  of  its  right 
border,  and  without  any  dilatation  of  the  left  ventricle.  This 
statement  implies  that  the  main  factor  in  the  causation  of  the 
rotation  is  an  increase  in  the  size  of  the  right  ventricle  towards 
the  left,  for  our  observations  seem  to  show  that  there  is  no 
increase  in  the  other  directions.  Its  right  boundary  is  normal, 
its  posterior  boundary — the  interventricular  septum — is  normal, 
for  the  left  ventricle  is  not  enlarged.  Its  lower  boundary 
is  normal,  limited  by  the  diaphragm.  Its  upper  border  can  be 
neglected  in  this  connection,  because  the  study  of  our  cases 
shows  clearly  that  upward  dilatation  occurs  without  any 
upward  displacement  of  the  apex.  As  regards  forward  in- 
crease the  presence  of  the  anterior  chest  wall  seems  to  prevent 
the  simple  bulging  forward  of  the  heart,  which  would  other- 
wise occur. 

There  only  remains,  therefore,  dilatation  of  the  right 
ventricle  to  the  left. 

It  is,  I  think,  demonstrable  that  a  dilatation  of  the  right 
ventricle  in  this  direction  may  well  cause  a  tilting  upwards 
of  the  apex.  To  allow  of  increase  in  this  direction  it  would  be 
necessary  for  the  left  ventricle  to  be  pushed  outwards  and 
backwards. 

Now  the  most  fixed  point  of  the  lieart  is  its  attachment  to 
the  diaphragm  (where  the  inferior  vena  cava  passes  through  that 
structure),  and,  as  has  been  already  pointed  out,  in  these  cases 
of  dilatation  of  the  right  ventricle,  there  is  no  evidence  of  any 
dilatation  of  the  right  auricle,  and  therefore  this  fixation  point 
is  not  interfered  with,  as  it  would  be,  were  the  tissues  of  the 
auricular  wall  stretched  by  dilatation  of  that  chamber. 

The  attachment  of  the  heart  by  its  vessels  to  the  structures 
which  form  the  roots  of  the  lungs  constitutes  a  second  fixation 
point,  so  far  as  rapidly  acting  and  not  too  powerful  distortmg 
forces  are  concerned,  and  it  is  this  fixation  point  with  which 
we  have  now  to  deal. 


UPWARD  DISPLACEMENT  OF  APEX  3B9 

The  fact  that  the  left  ventricle  is  fixed  by  the  connection 
between  the  aorta  and  pulmonary  artery  at  the  base  of  the 
heart  and  is  free  to  move  only  at  the  apex,  prevents  it  from 
making  room  for  the  right  ventricle  by  simply  moving  away  to 
the  left. 

The  left  ventricle  will  therefore  act  towards  the  right  as 
if  it  were  a  rigid  board  swinging  on  a  hinge  placed  at  the  base 
of  the  heart.  If  more  room  is  needed  to  the  right  of  this 
board  the  tip  of  the  board  will  have  to  travel  to  the 
left,  outwards,  in  the  arc  of  a  circle  whose  centre  is  the 
hinge. 

This  then,  is  the  mechanism  Avhereby  the  apex  of  the  heart 
is  carried  upwards.  If  the  left  ventricle  has  to  move  away 
to  the  left  to  make  room  for  an  increase  in  the  volume  of  the 
right,  any  movement  to  the  left  must  be  of  the  nature  of  a 
rotation,  for  the  apex  cannot  increase  its  distance  from  the 
fixed  point  at  the  base. 

The  interventricular  septum  acts  as  the  radius  of  a  circle, 
and,  on  swinging  to  the  left  to  allow  of  more  room  for  the  right 
ventricle,  must  carry  the  apex  of  the  heart  upwards  in  its 
attempt  to  carry  it  outwards. 

This  appears  to  be  the  true  explanation  as  read  from  the 
clinical  facts.  It  is  not,  perhaps,  what  might  have  at  first 
sight  have  been  expected  to  take  place.  The  natural  thing 
would  have  been  for  the  ventricle  to  increase  to  the  right  of 
the  sternum,  as  it  does  ordinarily  when  there  is  considerable 
dilatation  of  this  chamber.  Or  else  it  would  be  expected 
simply  to  bulge  forwards  against  the  anterior  chest  wall  and 
find  room  for  itself  by  simply  displacing  the  left  ventricle  a 
little  backwards.  This,  too,  does  not  appear  to  be  the  case, 
as  shown  by  the  clinical  facts. 

To  summarise:  The  apex  of  the  heart  may  be  displaced 
upwards  in  cases  of  antemic  dilatation  of  the  organ  by  means 
of  a  rise  in  the  average  level  of  the  diaphragm  upon  which  it 
rests,  or  by  means  of  a  simple  downward  extension  of  the  right 
ventricle  which  raises  the  apex  by  pressure  against  the 
diaphragm. 

Or,  thirdly,  the  apex  may  be  raised  in  consequence  of  the 
left  ventricle  being  swmig  outwards  and  upwards  (around  its 


360 


DISPLACEMENT  OF  THE  HEART 


basal  fixation  point  as  centre)  in  order  to  allow  of  an  increase 
in  the  right  vontiicle  towards  the  left. 

Another  cause  of  upward  displacement  of  the  apex  appears 
to  be  the  simple  shrinkage  in  the  size  of  the  heart,  which  is 
described  at  p.  50  as  accompanying  a  diminution  of  the 
total  volume  of  the  blood  in  active  circulation.  Such  an 
elevation  of  the  apex  beat  is  shown  in  figs.  42,  &c. 

The  following  case  shows  the  rapidity  with  which  a  rise 


Size  on  28 

"    29 

"  z:z. 

I.e. 

NoTTncil 

cardiac 

&re6b 


28  JT 

=  2^^Z 

-5Vz 
=  o 


Fig.  129. 

H.  H.,  aged  seventeen.    Acute  pneumonia.     Rapid  dilatation   of  heart 
with  upward  displacement. 


in  the  position  of  the  heart  may  come  on  in  an  adolescent 
when  the  pulmonary  circulation  is  interfered  with  by  pneumonic 
consolidation. 

H.  H.,  aged  seventeen.  Taken  ill,  June  25,  at  9  a.m.,  with 
abdominal  pain  and  vomiting.  On  admission  to  hospital  next 
day,  he  had  severe  pain  in  the  right  iliac  region,  the  muscles  on 
the  right  side  of  the  abdomen  were  rigid,  and  he  was  supposed  to 
have  appendicitis.  The  pain  was,  as  the  result  proved,  really 
due  to  a  right  basal  pleurisy  which  gave  no  signs  at  first.  The 
lungs  which  were  clear  forty-eight  hours  after  the  onset  of  his 
illness,  rapidly  became  consolidated,  and  by  the  evening  of  the 
second  day  the  right  lower  lobe  was  affected,  and  on  the  third 
day  the  left  apex,  the  left  lower  lobe,  and  half  of  the  right  lower 


UPWARD  DISPLACEMENT   OF  APEX  361 

lobe  were  consolidated.  On  this  day  (June  28),  the  cardiac 
dullness,  which  on  the  previous  day  was  normal,  was  as  follows  : 
upper  border  at  the  second  rib,  left  border  at  the  nipple  line  in 
the  second  interspace,  and  in  the  fourth  interspace  it  was  at  the 
mid-axillary  line,  5|  inches  from  the  sternum.  The  lower 
border  of  the  heart  was  at  the  fifth  rib.  The  right  border  of 
the  heart  was  at  the  right  edge  of  the  sternum.  Two  days  later, 
when  the  dilatation  of  the  heart  was  less  extreme,  it  assumed 
the  state  which  is  typical  of  the  condition  we  are  describing. 
Its  upper  border  was  at  the  second  rib,  and  its  lower  border  at 
the  fifth.  Its  right  border  was  1  inch  to  the  left  of  the  sternum, 
and  its  left  border  was  nearly  an  inch  external  to  the  left  nipple 
line.  At  this  time  the  whole  of  the  left  lung  was  consolidated 
and  the  lower  half  of  the  right  lower  lobe  also  {vide  fig.  129). 
But  most  cases  of  cardiac  displacement  are  due  to  changes 
in  the  surrounding  viscera. 

II.  Extrinsic  Causes  of  Displacement 

The  heart  may  be  pushed  or  pulled  out  of  place  by  alterations 
in  the  volume  of  the  lungs,  or  of  the  abdominal  organs,  or  it 
may  be  displaced  by  the  growth  of  tumours  in  the  thorax 
or  abdomen. 

The  displacement  may  take  place  in  any  of  the  six  directions 
in  which  a  body  is  free  to  move  in  this  space  of  three  dimen- 
sions which  is  the  characteristic  of  our  universe.  I  shall  base 
my  classification  of  cardiac  displacements  upon  the  direction 
of  the  displacement,  and  in  the  following  order  :  (1)  forwards  ; 
(2)  backwards  ;  (3)  downwards  ;  (4)  upwards  ;  (5)  to  the  left ; 
(6)  to  the  right. 

1.  Displacement  Forwards.  —  The  normal  position  of 
the  heart  is  such  that  no  considerable  amount  of  forward  dis- 
placement is  possible,  although  aneurysm  or  tumour  in  the 
posterior  mediastinum  would  cause  rather  more  of  the  heart 
than  normal  to  come  into  contact  with  the  anterior  chest 
wall. 

2.  Displacement  Backwards. — This  is  of  course  frequent 
in  emphysema,  where  it  occurs  in  combination  with  displacement 
downwards,  as  a  result  of  the  over-distension  of  the  lungs, 
and  especially  of  the  thin  margins  which  overlie  the  heart. 
A  certain  amount  of  displacement  backwards  also  frequently 


362  DISPLACEMENT  OF  THE  HEART 

results  from  compensatory  enlargement  of  the  right  lung  which 
accompanies  disease  confined  to  the  left  one. 

Also,  as  was  pointed  out  when  reference  was  made  to  the 
smallness  of  the  area  of  the  cardiac  dullness  in  cases  of  myo- 
cardial weakness  in  distensible  hearts,  a  certain  amount  of 
the  apparent  smallness  of  the  heart  when  the  patient  lies  back 
may  be  due  to  the  underfilled  heart  not  being  large  enough 
to  come  into  as  close  contact  with  the  anterior  chest  wall  as 
a  full  heart  would. 

It  is  possible  also  that  there  may  be  some  backward  dis- 
placement as  well,  but  it  is  a  point  of  no  importance. 

Cases  showing  this  diminution  of  the  cardiac  dullness  are 
given  at  pp.  118,  183,  196,  &c. 

3.  Downward  Displacement  of  the  Heart  Owing  to 
Abnormal  Lowness  of  the  Diaphragm 

Downward  displacement  of  the  diaphragm  will  result  when- 
ever the  volume  of  the  thoracic  contents  is  considerably 
increased. 

This  is  most  commonly  observable  when  there  is  a  consider- 
able accumulation  of  liquid — whether  of  sermn  or  of  pus — in 
either  pleural  cavity.  The  marked  downward  displacement  of 
the  liver  in  such  cases  is  satisfactory  evidence  of  this  alteration 
in  the  level  of  the  diaphragm.  Another  common  cause  of 
over-filUng  of  the  thorax  is  where  the  volume  of  the  lungs  is 
permanently  increased  as  a  result  of  their  over-distension  by 
frequent  coughing  in  the  condition  known  as  emphysema. 
Then,  as  is  well  known,  not  only  is  the  horizontal  measurement 
of  the  chest  increased  giving  it  the  classical  '  barrel  shape,' 
but  its  floor  is  also  lowered,  and  the  resonance  of  the  lungs 
is  found  to  extend  to  a  lower  level  than  normal.  The  lowness 
of  the  diaphragm  is  not  only  shown  by  percussion  of  the  upper 
border  of  the  hver,  but  also  by  the  increased  accessibility  of  the 
heart  to  palpation  in  the  epigastrium. 

Another  common  cause  of  dowiiward  displacement  of  the 
heart,  due  to  the  lowering  of  the  diaphragm  (upon  which  it  rests), 
is  not,  I  believe,  so  generally  recognised  as  those  ah'eady  men- 
tioned, and  it  must  therefore  be  dealt  with  a  little  more  fullv. 


DISPLACEMENT  ])OWNWARDS  363 

In  this  case,  the  overfilHng  of  the  thorax  is  due  to  excess 
of  the  fluids  normally  present  in  it. 

We  have  spoken  of  downward  displacement  from  the 
abnormal  presence  of  watery  fluid  in  the  pleura  and  from 
abnormal  distension  of  the  Imigs  by  air,  and  we  now  have  to 
speak  of  downward  displacement  of  the  diaphragm  and  heart 
by  the  persistent  presence  of  an  abnormal  amount  of  blood  in 
the  thorax. 

Li  such  cases  as  severe  mitral  stenosis,  where  the  heart 
muscle  is  strong,  we  Imow  that  there  is  chronic  engorgement 
of  the  lungs  with  blood  and  also  chronic  over-distension  of  the 
great  veins. 

If  a  series  of  such  cases  be  carefully  examined  it  will  be 
found  that  downward  displacement  of  the  diaphragm  and 
heart  occurs  too  frequently  to  be  a  mere  coincidence. 

In  valvular  disease  wuth — what  appears  to  be — a  considerable 
dilatation  of  the  heart  towards  the  epigastrium  and  consider- 
able downward  enlargement  of  the  liver,  it  is  not  infrequently 
possible  to  demonstrate  that  the  epigastric  pulsation  must  be 
in  part  due  simply  to  downward  displacement  of  the  heart,  and 
that  part  of  what  appears  to  be  enlargement  of  the  liver  must 
also  be  simply  downward  displacement  due  to  the  lowness  of 
the  diaphragm. 

The  theoretical  considerations  in  connection  with  the 
elevation  of  the  diaphragm  which  occurs  in  cases  wdiere  the 
amount  of  blood  in  the  thorax  is  less  than  normal  have  already 
been  dealt  with  in  Essay  II,  p.  163. 

The  proposition  here  made  is  the  simple  converse  of  that, 
and  the  careful  percussion  of  the  liver  and  the  auscultation  and 
percussion  of  the  heart  in  a  series  of  cases  where  there  is  well- 
marked  venous  plethora  (the  result  of  chronic  valvular  disease 
with  imperfect  compensation)  will  clearly  demonstrate  the 
accuracy  of  what  is  here  stated — namely,  that  chronic  venous 
engorgement  of  the  lungs  and  the  thoracic  veins  does  lead  to  a 
lowering  of  the  diaphragm,  and  consequently  to  a  downward 
displacement  of  the  heart  w4iich  rests  upon  it.  For  careful 
percussion  and  auscultation  wall  show  that  the  upper  level  of 
the  hver  dullness  is  often  lower  than  normal  in  these  cases, 
and  that  the  upper  border  of  the  heart — as  judged  both  by 


361 


DISPLACEMENT  OF  THE  HEART 


percussion  and  by  the  point  of  maximal  intensity  of  the 
puhiionary  second  somid — is  also  lower  than  normal. 

A  slight  case  of  this  nature  is  given  at  p.  218,  where  the 
venous  plethora  was  presumably  due  to  overstrain  of  the  heart 
apart  from  valvular  disease. 

The  following  is  a  well-marked  case  of  this  nature  where 


Low  Diaphragm  due  to  Chronic  Over-distension  of  the 
Lungs  and  Thoracic  Veins  avith  Blood 


Normal  level 

o£  aJbsolute 

liver  dulness. 

Liver  _ 
dulness 


\P.If.l  of 
jpulm? 


space 
.line 
Area  of 
'■Relaliive  & 
FuUg-astric 
resonance 
oi&ca,inable 
thron^h  the 
liver 


Fig.  130. 

Arthur  H.  P.,  aged  thirty.    Mitral  stenosis.      Downward  displauemcut  of 
the  heart  by  long  continued  chronic  venous  congestion. 


the  lowness  of    the  whole  heart   was   also   conlirmed    by   a 
radiograph. 

It  is  a  most  striking  case,  as  will  be  seen  by  studying  hg.  130 
together  with  the  actual  photographs  of  the  patient's  chest. 
Previous  to  taking  the  photographs,  the  outhne  of  the  cardiac 
area  and  the  liver  dullness  were  marked  on  the  chest  in  ink, 
and  also  the  areas  over  which  the  pulmonary  second  sound 
and  the  cardiac  murmur  were  audible,  as  well  as  the  area  over 
which  the  right  ventricular  impulse  was  best  felt  {mde  Plates 


Dow.ws  ai:d  Displacement  of  the  Diaphragm  and   He.uit   owing  to  Chronic 
Over-distension  of  the  Thoracic  Viscera  with  Blood. 


Arthur  H.  P.,  mitral  stenosis.  Pliotograpli  of  the  chest,  showing  the  outline  of  the  viscera  as  deter- 
mined by  percussion  when  recumbent.  Note  the  close  correspondence  between  the  actual  lines  as  drawn 
on  the  chest  and  the  diagram  shown  in  fig.  130.  Note  the  lowness  of  the  cardiac  area,  also  the  way 
in  which  the  gastric  resonance  is  obtainable  through  the  Uver  owing  to  the  increased  conductivity  to 
percussion  vibrations  which  results  from  its  over-distension  with  blood. 


PLATE  V 


l)u\\  N\v.uiD   Displacement   of  the  Diaphragm  and   Heart   owing  to   Chronic 
Over-distension  of  the  Thoracic  Viscera  with  Blood. 

Arthur  H.  P.,  mitral  stenosis.     Lateral  view  of  the  chest  showing  the  outline  of  the  viscera  as  determuied 
by  percussion,  when  recumbent.    Note  the  downward  and  outward  displacement  of  the  heart. 


Downward    Displacement    of   the    Diaphracm    and    Heart,    the    result    of 
Chronic  Over-distension  of  the  Thoracic  Viscera  with  Blood. 

Arthur  H.  V.,  mitral  stenosis.  Kailiosrapli  taken  with  tlie  patient  lying  on  his  face.  The  position  of 
the  fourtli,  fiftli,  sixtii,  and  seventh  ribs  anteriorly  was  marlved  by  strips  of  lead. 

Note  tliat  the  main  bulk  of  the  heart  is  below  the  fifth  rib,  thus  confirming  the  cUnical  observation 
that  the  pulmonary  valves  were  below  the  fourth  rib.  Note  the  shadow  of  the  dilated  right  auricle  lying 
between  the  fifth  and  seventh  ribs  (instead  of  between  the  third  and  fifth),  also  the  absence  of  shadow  in  the 
seventh  right  interspace  showing  the  presence  of  lung  at  that  level  and  the  lowness  of  the  diaphragm. 

The  outer  ends  of  the  lead  strips  marking  the  sixth  and  seventh  ribs  have  slipped  out  of  place  and  lie 
at  too  low  a  level. 


DISPLACEMENT  DOWNWARDS  365 

IV  and  V).     The  displacement  is  also  shown  by  the  radiograph 
reproduced  in  Plate  VI. 

The  patient  was  a  man  aged  thirty,  an  engi-aver  by  trade, 
who  had  had  '  rheumatic  fever  '  three  times  before  he  was  seven 
years  old,  and  not  at  all  since,  although  he  had  often  suffered 
from  rheumatic  pains. 

As  a  lad,  he  had  no  dyspnoea,  and  played  football  and  hockey. 
His  present  cardiac  incapacity  began  some  two  and  a  half  years 
ago,  with  sudden  very  sharp  pain  in  the  left  prsecordium.  He 
got  better  after  some  months,  and  was  able  once  again  to  play 
cricket ;  but  then  a  fall  which  dislocated  his  shoulder  made  him 
worse  again,  and  he  has  been  breathless  ever  since.  For  some 
months  now,  fresh  symptoms  have  come  on  instead  of  the  breath- 
lessness.  He  is  now  prevented  from  exerting  himself  much  by 
a  sense  of  swelling  in  the  epigastrium  accompanied  by  palpita- 
tion, which  forces  him  to  rest  mitil  it  passes  off.  Also  his  legs 
and  arms  and  even  his  body  go  cold  on  exertion — even  in  warm 
weather.  After  he  has  walked  a  quarter  of  a  mile  or  so,  he 
often  has  to  stop  because  of  this  coldness,  and  after  resting  five 
minutes  or  so  his  feet  and  legs  go  warm  again.  He  has  no  leg 
pains  on  exertion  {vide  p.  469), 

The  examination  of  the  heart  showed  he  was  suffering  from 
mitral  stenosis  with  evident  signs  of  faulty  compensation. 

The  cardiac  area  was,  however,  much  lower  than  normal,  and 
the  lower  margin  of  the  lungs  was  also  very  greatly  below  the 
usual  level — as  reference  to  the  illustrations  will  show. 

The  cardiac  pulsation  and  dullness  extended  from  the 
fourth  rib  down  to  the  eighth  rib,  and  the  amount  of  cardiac 
dilatation  was  also  shown  by  the  fact  that  the  cardiac  area 
stretched  from  1|  inches  to  the  right  of  the  sternum  in  the 
fourth  interspace  to  the  left  anterior  axiUary  Hne  in  the  seventh. 

At  first  sight  it  would  be  thought  that  the  presence  of  the 
apex  beat  in  the  seventh  interspace  in  the  anterior  axillary  Line 
would  mean  that  the  heart  was  enormously  dilated.  On  noting 
the  base  of  the  heart,  however,  it  was  found  that  the  cardiac 
dullness  did  not  extend  above  the  fourth  rib,  and  that  the  point 
of  maximal  loudness  of  the  pulmonary  second  sound  was  in  the 
fourth  left  interspace  instead  of  the  second.  This  fact  pointed 
towards  downward  displacement  of  the  heart  owing  to  descent 
of  the  diaphragm.  On  examining  the  liver  dulhiess  to  find  if 
there  were  any  other  evidence  of  a  low  diaphragm,  strong  con- 
firmatory evidence  was  forthcoming,  for  the  edge  of  the  right 


360 


DISPLACEMENT  OF  THE  HEART 


lung  came  down  to  within  one  inch  of  the  costal  arch  and 
crossed  the  eighth  rib  in  the  nipple  hne  instead  of  the  sixth. 
The  relative  dullness  of  the  liver  was  at  the  seventh  rib  in  the 
right  nipple  line  instead  of  the  fifth.  Posteriorly,  the  same 
phenomenon  was  observable,  for  the  lungs  came  do^^^l  to  below 
the  twelfth  rib  on  both  sides. 

There  was  nothing  in  the  patient's  history  to  explain  the 
abnormal  size   of  the    lungs,  for  he  could  not  take  violent 

exercise  and  had  never 
^^'^~''^'  ^  suffered    from    bron- 

chial trouble.  Once, 
four  years  ago,  he 
liad  a  cough  brought 
on  by  exertion,  but  it 
subsided  in  a  few  days. 
Therefore,  there  was 
no  reason  to  suspect 
the  presence  of  em- 
physema ;  and  the 
probability  is  that  the 
low  diaphragm  is  a 
result  of  the  chronic 
engorgement  of  the 
lungs  and  not  a  mere 
coincidence. 


^^  ext.  to 
V.N.L. 


Fig.  131. 


Show- 


George  G.,  December  1904.  ilitral  stenosis, 
ing  the  size  and  position  of  the  heart  during  twelve  years 
1892-1904,  while  compensation  remained  good  and 
there  was  no  evidence  of  congestion  of  the  lungs. 


Two     figures     are 
given  of  another  case 


showing  how  much 
the  level  of  the  heart  dropped  in  the  course  of  seven  years — 
namely,  figs.  131  and  132. 

The  case  was  one  of  pure  mitral  stenosis  with  such  an 
extreme  degiee  of  narrowing  that  even  when  compensation 
was  at  its  best  and  the  patient  able  to  get  about  fairly 
well  there  wag  a  very  loud  pre-systolic  murmur  and  thrill 
as  well  as  a  very  loud  mid-diastoHc  mitral  murmur.  For 
twelve  years,  from  1892  till  1904,  while  the  patient  was  com- 
paratively well  and  able  to  work,  the  apex  remained  in  the 
fifth  interspace  in  about  the  nipple  line.  As  a  rule,  during  this 
period,  there  was  no  evidence  of  chronic  venous  congestion 
of  the  lungs. 

Two  drawings  are  given  :  one  sliowing  the  size  and  position 


DISPLACEMENT  DOWNWARDS 


367 


of  the  heart  in  December  1904  to  have  been  normal  except 
that  the  apex  was  just  external  to  the  nipple  line.  The 
second  one  shows  the  condition  of  the  heart  seven  years  later — 
namely,  November  1911,  when  it  was  displaced  downwards. 

There  are  distinct  evidences  of  displacement  downwards, 
although  the  drop  of  the  apex  beat  from  just  external  to  the 


T.KI 


^Area  of 

loxudness 
ofpulmonY 
'sound 

Tzdd.Zine 


Fig.  132. 

George  G.  Mitral  stenosis,  Xovember  1911.  Showing  doxNTiward 
displacement  of  the  heart  and  enlargement  of  the  liver  due  to  some 
years  of  chronic  venous  congestion  from  failing  compensation. 


nipple  line  in  the  fifth  space,  to  the  sixth  interspace  one  inch 
external  to  the  nipple  hne,  might  well  be  accounted  for  by 
simple  dilatation  and  hypertrophy.  The  falling  of  the  point 
of  maximal  loudness  of  the  aortic  and  pulmonary  second 
sounds,  however,  from  the  second  to  the  fourth  interspaces, 
is  very  suggestive  of  displacement,  as  is  also  the  descent  of 
the  upper  edge  of  the  liver  dullness  from  the  sixth  rib  to  the 
seventh.  For  some  years  prior  to  1911,  compensation  had 
been  failing. 

Displacement  of  the  heart  downwards  will  also  result  from 


368  DISPLACEMENT  OF  THE  HEAET 

the  growth  of  tumours  m  the  thorax  if  of  sufficient  size — as  in 
the  case  of  endotheHoma  of  the  pleura  or  mediastinal  lympho- 
sarcoma. 

4.  Displacement  of  the  Heart  Upwards. — As  the  heart 
lies  upon  the  central  tendom  of  the  diaphragm,  anything  which 
causes  the  ascent  of  that  structure  will  raise  the  heart  to  a 
higher  level  in  the  thorax  than  normal.  Anything  increasing 
the  intra-abdominal  pressure  sufficiently  to  raise  the  diaphragm 
will  therefore  cause  upw^ard  displacement  of  the  heart.  This 
occurs  in  the  case  of  ascites,  or  the  abdominal  distension  of 
peritonitis,  enteric  fever,  &c.  More  important  from  the  cHnical 
point  of  view  is  the  upward  displacement  of  the  heart  which 
is  brought  about  by  flatulent  distension  of  the  stomach,  because 
this  is  very  often  seen  in  heart  failure,  as  a  consequence  of 
faulty  circulation,  and  the  additional  cardiac  embarrassment 
caused  thereby  may,  when  life  is  trembling  in  the  balance, 
turn  the  scale  against  recovery. 

But  the  diaphragm  does  not  only  rise  as  a  result  of  pressure 
from  below,  it  may  also  undoubtedly  be  drawn  upwards  by  a 
diminution  in  the  volume  of  the  intrathoracic  contents.  As  to 
the  nature  of  this  diminution,  I  am  not  at  present  prepared  to 
dogmatise.^  It  may  sometimes  be  due  mainly  to  a  diminution 
in  the  size  of  the  lungs  owing  to  changes  following  upon  altera- 
tions in  the  respiratory  functions,  as  in  the  cases  of  chlorosis  ; 
but  it  is  in  my  opinion  certainty  due,  sometimes,  to  a  diminution 
of  the  total  volume  of  the  blood  which  the  heart  is  able  to  put  in 
circulation.  For  instance,  in  a  case  of  sudden  cardiac  failure — 
such  as  from  an  influenzal  affection  of  the  heart — the  diaphragm 
can  be  observed,  in  the  course  of  a  day  or  so,  to  rise  to  an  inch 
or  more  above  its  normal  position,  carrying  the  lower  border 
of  the  heart  up  to  above  the  level  of  the  fifth  rib  in,  and  internal 
to,  the  nipple  line  on  the  left  side. 

The  following  is  an  instance  of  such  a  case  : — 

A  young  man,  aged  about  twenty-eight,  in  good  health,  was 
suddenly  seized  with  severe  abdominal  pain  of  a  colicky  nature, 
accompanied  by  syncopal  attacks,  in  the  first  of  which  his  pulse 
rate  fell  to  below  40  per  minute.     The  heart  remained  very 

'  The  greater  part  of  this  essay  was  written  in  1901.      See    Birmingham 
Medical  Review,  October  1901.     Compare  also  Essay  IT. 


DISPLACEMENT  UPWARDS 


369 


feeble,  and  some  ten  days  or  so  after  the  onset  of  his  illness, 
the  cardiac  dullness  was  greatly  diminished  in  area,  and  its 
lower  level  did  not  reach  below  the  fifth  rib.  Although  there 
was  not  the  least  sign  of  any  gastric  distension,  full  gastric 
resonance  was  obtamablc  up  to  the  fifth  rib  in  and  internal  to 
the  left  nipple  line,  and  in  the  middle  hne  under  the  sternum 
full  gastric  resonance  was  obtainable  up  to  the  level  of  the  fifth 
rib,  and  full  pulmonary  resonance  above  it.  To  the  right  the 
liver  was  one  interspace  higher  than  normal.  As  the  heart  got 
stronger,  the  liver  and  the  stomach  returned  to  their  usual  level. 


Fig.  133. 

Normal    Percussion    of    Heart, 
Liver,  and  Stomach. 


Fig.  134. 

Showing  Displacement  Upwards 
OF  Heart,  Liver,  and  Stomach. 


In  both  figures  the  close  shading  represents  absolute  dullness  and  the  light  shading  relative 
dullness.    The  area  of  gastric  resonance  is  outhned  and  left  unshaded. 

showing  that  the  diaphragm,  and  with  it  the  heart,  had  also 
returned  to  its  normal  position  (see  fig.  41,  p.  183). 

Another  condition  in  which  this  upward  displacement  of 
the  heart  (due  to  the  ascent  of  the  diaphragm)  is  observable,  is 
where  it  may  reasonably  be  supposed  that  there  is  a  diminution 
in  the  total  volume  of  the  blood  in  circulation.  Thus  I  have 
seen  it  more  than  once  in  enteric  fever  accompanied  by  a 
hollowing  of  the  abdomen  and  a  shrinkage  of  the  limbs  and 
face — evidently  pointing  to  a  diminution  of  the  circulating 
fluids  of  the  body,  fi'om  failure  of  absorption  of  nourishment. 

2  B 


370 


DISPLACEMENT  OE  THE  HEART 


A  very  marked  case,  of  ^^■bicll  1  now  give  some  particulars, 
occurred  in  a  young  woman  imder  treatment  for  gastric  ulcer 
with  a  suspicion  of  impending  perforation.  The  diminution 
in  the  supply  of  nomishment,  necessitated  by  rectal  feeding, 
brought  about  the  following  condition  {vide  fig.  134). 

A.  v.,  aged  twenty-one,  '  was  fed  mainly  by  the  bowel  until 
thi'ee  or  four  days  ago.     The  gastric  resonance  to-day  reaches 

up  to  the  upper  border 

Upward  Displacement  of  the  Heart  by         of  the  fifth  rib  in  and 

High  Diaphragm  internal     to     the     left 

nipple  Hne,  and  there 
is  no  dullness  at  all  in 
the  fifth  interspace. 
The  lower  border  of 
the  hver  in  the  middle 
Hne  does  not  reach 
as  low  as  the  tip  of 
the  xiphoid  cartilage, 
and  in  the  right  nipple 
hne  the  relative  dull- 
ness of  the  hver  com- 
mences at  the  fourth 
rib,  and  the  absolute 
dullness  at  the  fifth  rib, 
while  the  lower  edge 
of  the  hver  does  not 
seem  to  reach  lower 
than  the  sixth  inter- 
space as  there  is  full 
intestinal  resonance  below  this  level.  In  the  mid-axillary  hne 
intestinal  resonance  reaches  as  high  as  the  eighth  mterspace, 
and  the  lower  edge  of  the  lung  only  comes  down  to  the  lower 
border  of  the  sixth  rib.'  The  condition  is  shown  in  fig.  134, 
and  a  nonnal  chest  is  shown  in  fig.  133  for  comparison  with  it. 

Fig.  135  also  shows  a  well-marked  case  of  this  nature 
occurring  in  a  lady  aged  thuty-one,  who,  because  of  pain,  had 
greatly  hmited  the  amount  of  food  she  took,  but  had  at  the 
same  time  continued  to  hve  an  active  hfe.  The  chief  symptom 
besides  her  pain  was  a  feeling  of  undue  weariness.  Considering 
the  condition  of  her  circulation  such  a  symptom  could  easily 
be  understood  (see  also  Essay  II). 


Fig.  135. 

Nurse  T.,  aged  thirty-one,  October  30,  1913.  Upward 
displacement  of  the  heart  by  high  diaphragm  due 
to  malnutrition  accompanying  mucus  colitis.  Ko 
murmurs. 


LATERAL  DISPLACEMENT  371 

It  is  presumably  possible  iur  the  apex  to  bo  raised  by 
other  extrinsic  agencies,  such  as  by  traction  by  pleural  ad- 
hesions when  the  pericardium  is  adherent ;  but  such  are  not 
often  met  with  and  are  of  httle  clinical  importance. 

Latekal  Displacement  of  the  Heart 

Before  taking  up  the  question  of  lateral  displacement  of 
the  heart,  it  will  be  well  to  say  a  few  words  as  to  the  mobility 
of  the  heart.  Careful  clinical  observation  seems  to  show 
clearly  that  it  is  not  correct  to  regard  the  heart  as  being  '  fixed  ' 
in  its  position  by  the  fibrous  tissue  which  surrounds  the  aorta 
and  the  roots  of  the  lungs,  nor  yet  by  the  attachment  of  the 
inferior  cava  to  the  diaphragm. 

^  These  points  of '  fixation  '  must  only  be  regarded  as  relative 
and  not  absolute,  for,  even  in  adult  life  (when  the  fibrous 
tissues  may  be  regarded  as  having  attained  to  a  full  degree  of 
firmness)  the  heart  and  the  tissues  of  the  mediastinum  can 
shift  from  their  position  in  the  middle  fine  of  the  body  and 
travel  either  to  the  left  or  to  the  right,  if  one  or  other  of  the 
lungs  collapses,  and  the  other  becomes  compensatorily  enlarged, 
and  the  apex  of  a  heart  of  normal  size  may  be  found  as  far 
from  its  normal  situation  as  the  left  posterior  axillary  line  or 
the  right  anterior  axillary  fine. 

In  adolescence,  owing  to  the  softness  and  immaturity  of  the 
fibrous  tissues,  these  changes  in  the  position  of  the  heart  may 
take  place  with  almost  unbeHevable  rapidity,  as  in  the  following 
case  where  (owing  to  the  sudden  collapse  of  an  inflamed  left 
lung,  as  a  result  of  vaccine  treatment)  the  heart  in  the  course  of 
less  than  ten  days  shifted  over  some  tw^o  inches  to  the  left  of 
its  former  position,  so  that  its  right  border  was  almost  in  the 
left  nipple  Une  and  its  apex  in  the  axilla.  The  greater  part 
of  this  movement,  moreover,  took  place  in  the  course  of  only 
three  or  four  days. 

The  following  are  the  details  of  the  case. 

The  patient,  Lily  B.,  eighteen  years  of  age,  was  admitted 
to  the  General  Hospital,  under  Mr.  Haslam  (to  whom  I  am 
indebted  for  permission  to  refer  to  the  case),  in  January 
1908,  suffering  from  a  septic  condition  of  the  right  kidney. 

2  B  2 


372 


DISPLACEMENT  OF  THE  HEART 


In  spite  of  excision  of  the  kidney,  pysemia  developed.  The 
temperature  rose  to  103-6°  F.,  and  an  extensive  amount 
of  septic  pneumonia  developed — both  lungs  being  affected. 
The  left  one  was  most  involved,  and  there  were  many  areas 
of  dullness  and  tubular  breathing  scattered  throughout  the 
whole  of  the  lungs  with  very  numerous  Uquid  rales.  The 
lower  part  of  the  right  lower  lobe  was  similarly  affected.     It 


IJdge  of 
Jung-         /  \^^ 
on  5^-^=% 
on  e^^^Vz 

"      "  <3,hs. 
dulnessz"' 


\5"frozn. 


-  -    ^rh/\  [ sternum 


Fk!.  13G. 

Lily  B.,  agel  eigUteeu.  Kapid  displacement  of  tlie  Ueart  to 
tlxe  left  by  collapse  of  the  left  lung  on  the  arrest  of  pyasmic 
imeumoaia.  On  ilarch  5,  edge  of  right  luug  was  J  inch  to  left  of 
the  sternum.  On  Ifarch  6,  edge  of  right  limg  was  2  inches  to  left 
of  the  sternum.  Also  on  this  date  there  was  full  lung  resonance 
for  IJ  inches  to  the  left  of  the  sternum,  and  gastric  resonance  in 
the  fifth  space  to  the  anterior  axillary  line. 


was  certainly  a  case  of  septic  broncho-pneumonia,  and  the 
prognosis  was  very  grave  indeed  as  pysemic  abscesses  were — 
almost  certainly — on  the  point  of  forming  throughout  the 
lung.  At  my  suggestion,  an  exploratory  puncture  of  the  lung 
was  made,  and  it  was  found  that  the  infection  was  strepto- 
coccal in  nature,  and  an  autogenous  vaccine  was  prepared. 
A  first  dose  of  10  milhon  was  given  on  March  1,  and  a 
second  on  March  3,  together  with  100  milhon  staphjdococci 
obtained  from  the  operation  wound.  A  striking  improve- 
ment followed  the  first  injection  of  vaccine,  and  by  the  fifth 
of  March  there  was  a  great  change  in  the  condition  of  the  left 
lung.  The  upper  and  middle  lobe  on  the  right  side,  where 
there  had  been  some  patches  of  consolidation,  were  now  quite 


LATERAL  DISPLACEMENT  373 

clear,  but  there  was  still  some  consolidation  with  tubular  breath- 
ing at  the  base  of  this  lung.  As  regards  the  left,  the  whole  of 
this  lung  was  now  uniformly  consolidated,  and  there  were 
numerous  moist  rales.  But  this  increased  consolidation  was 
shown  not  to  bo  due  to  fresh  pneumonic  infiltration  by  the  fact 
that  the  heart  was  being  drawn  and  pushed  towards  this  side, 
for  the  right  lung  now  crossed  over  and  its  edge  could  be 
detected  |  inch  to  the  left  of  the  sternum.  This  condensa- 
tion and  shrinkage  of  the  left  lung  progressed  so  rapidly  that 
next  day  the  edge  of  the  right  lung  was  fully  2  inches  to  the 
left  of  the  sternum,  during  inspiration,  from  the  first  rib  down 
to  the  fifth,  and  for  1|  inches  to  the  left  of  the  sternum 
there  was  no  cardiac  dullness  at  all.  Both  lungs  also  were 
clearing  very  satisfactorily,  and  there  were  hardly  any  rales  to 
be  heard.  Next  day,  March  7,  the  heart  had  moved  still  farther 
towards  the  left,  and  its  right  border  was  nearly  2  inches  from 
the  sternal  edge,  and  edge  of  the  right  lung  was  nearly  in  the 
left  nipple  line — i.e.  some  2|-  inches  to  the  left  of  the  sternum. 
The  apex  of  the  heart  was  nearly  in  the  anterior  axillary  hne — 
more  than  2  inches  to  the  left  of  the  position  it  had  occupied 
three  or  four  days  previously.  It  was  now  4|  inches  from  the 
sternum,  or  5^  from  the  middle  line  (see  fig.  136). 

The  reason  for  this  sudden  movement  of  the  heart  was 
what  we  may  call  the  collapse  of  the  left  lung  due  to  the  sudden 
cessation  of  the  inflammatory  process  brought  about  by  the 
vaccine  treatment. 

In  the  course  of  a  few  weeks  the  left  lung  re-expanded  and 
the  heart  returned  to  its  normal  situation. 

The  case  has  been  published  by  Dr.  Wynn,  in  its  bacterio- 
logical aspect,  as  he  had  charge  of  the  vaccine  treatment. 

In  this  girl,  therefore,  the  whole  heart  shifted  over  fully 
2  inches  to  the  left  of  its  previous  position  in  the  com-se  of  a  few 
days  only,  and  with  such  a  case  as  this  before  us,  we  cannot 
speak  of  the  heart  being  '  fixed  '  in  its  normal  position  unless 
we  use  the  term  as  a  relative  one  only. 

We  now  have  to  deal  with — 

5.  Displacement  of  the  Heart  to  the  Left. — Dis- 
placement of  the  heart  to  one  side  or  the  other  is  of  extremely 
common  occurrence  in  diseases  of  the  lungs  and  pleura,  and 
the  presence  and  amount  of  the  displacement  is  often  of  the 
greatest  clinical  value  from  a  diagnostic  point  of  view. 


371  DISPLACEMENT  OF  THE  HEART 

►'  I  need  not  point  to  the  well-known  displacement  of  the 
heart  which  occurs  in  extreme  plem-itic  effusion  or  in  empyema. 
Its  significance  has  long  been  recognised  and  appreciated. 

In  these  cases  the  heart  is  pushed  out  of  place  by  the  pressure 
of  the  accumulated  fluid.  But,  as  in  the  last  case,  the  heart 
may  not  only  be  pushed  out  of  place  by  excess  of  pressure 
on  one  side  of  the  thorax,  but  it  may  also  be  drawn  out  of 
place  by  the  traction  of  a  lung  which  is  shrinking  and  becoming 
fibrosed  as  a  result  of  chronic  inflammation,  or  from  other 
cause,  or  by  the  traction  exerted  by  the  absorption  of  pleuritic 
fluid  when  the  lung  is  too  much  damaged  to  expand  again. 
It  is  possible  to  produce  a  far  greater  amount  of  cardiac  dis- 
placement in  this  way  by  traction  of  one  lung  (combined 
with  a  compensatory  enlargement  of  the  other)  than  in  the 
first-mentioned  way,  by  means  of  pressm'e. 

It  may  be  of  interest  not  only  to  give  some  well-marked 
cases,  such  as  that  figured  on  p.  167  and  that  which  now  follows, 
but  also  some  illustrating  the  value  to  the  clinician  of  this 
cardiac  displacement. 

It  would  be  easy  to  give  many  cases  where  great  displace- 
ment of  the  heart  to  the  left  resulted  from  the  cicatricial 
contraction  of  a  lung  that  has  healed  after  some  inflammation, 
liut  the  following  case  only  will  be  given  : — 

Miss  W.,  aged  about  twenty-six,  was  brought  to  me  by  her 
doctor  on  account  of  cardiac  dilatation,  because  she  was  rather 
breathless  and  the  heart's  apex  was  in  the  axilla.  On  examining 
the  chest  it  was  found  that  the  heart's  apex  was  external  to  the 
anterior  axillary  line,  and  the  cardiac  dullness  and  pulsation 
reached  nearly  to  the  anterior  axillary  line  in  the  third  inter- 
space. But  on  percussing  out  the  right  border  of  the  heart  it 
was  found  to  be  nearly  in  the  left  nipple  fine,  and  that  the  right 
lung  crossed  to  about  2  inches  to  the  left  of  the  sternum. 
On  examining  the  chest  it  was  evident  that  the  left  lower  lobe 
was  almost  completely  fibrosed,  and  the  right  lung  crossed  over 
the  middle  line  to  the  extent  of  1|  inches  or  more.  There  was 
no  history  of  ilhiess  or  of  expectoration,  and  the  destructive 
process — a  tubercular  one — had  gone  on  to  this  extent  without 
the  knowledge  of  the  patient  or  the  doctor  who  had  seen  her 
occasionally. 

Cases   showing  such  an    extrerao   degree  of  displacement 


LATERAL  DISPLACEMENT  375 

are  of  interest  clinically,  because  they  show  the  completeness 
of  nature's  efforts  to  cure  by  the  absorption  and  cicatricial 
contraction  of  the  diseased  lung  tissue.  They  have  not, 
however,  the  same  clinical  and  diagnostic  importance  which 
the  slighter  cases  have,  where  the  recognition  of  a  slight  amount 
of  cardiac  displacement  may  throw  important  light  upon  the 
diagnosis  and  treatment  of  the  case. 
The  following  is  such  a  case — 

Charlotte  D.,  aged  forty-four,  admitted  to  the  General 
Hospital  with  left  pleural  effusion.  Her  doctor  had  tapped  her 
chest  three  weeks  previously  and  drawn  off  clear  serum,  but  it 
had  apparently  reaccumulated,  and  he  therefore  sent  her  to  the 
hospital  for  further  treatment.  The  left  base  was  dull  with 
diminished  breath  sounds,  &c.,  as  far  up  as  the  angle  of  the 
scapula,  and  exploratory  puncture  showed  the  presence  of  serum 
in  the  left  pleura.  The  question  now  arose  as  to  the  need  for 
again  tapping  the  pleura,  the  breathing  being  considerably 
embarrassed,  and  the  amoimt  of  dullness  suggesting  a  not  in- 
considerable pleuritic  effusion.  On  percussing  the  heart, 
however,  it  was  found  that  the  right  border  of  the  cardiac 
dullness  did  not  reach  the  left  edge  of  the  sternum,  because 
the  resonance  of  the  right  lung  crossed  over  to  the  left  of 
the  middle  hne  as  far  as  midway  between  the  sternal  edge 
and  the  left  nipple  Hne.  The  left  border  of  the  heart  was 
also  displaced  one  inch  or  so  to  the  left  of  its  normal  position. 
From  this  shght  displacement  of  the  heart  towards  the  pleural 
effusion  it  was  evident  that  absorption  was  going  on  as  fast  as 
possible,  and  that  there  was  already  what  might  almost  be  called 
a  negative  pressure  in  the  left  pleural  cavity.  The  reason  for 
the  non-absorption  of  the  fluid  was  the  inabiUty  of  the  lung 
to  expand,  and  further  tapping  could  do  no  good.  The  case 
was  treated  by  respiratory  exercises  with  a  view  to  aiding  the 
expansion  of  the  lung  with  a  satisfactory  result. 

Another  case  illustrating  the  value  of  a  careful  mapping 
out  of  the  right  border  of  the  heart  is  that  shown  in  fig.  137. 

It  is  the  case  of  a  man,  aged  fifty-eight,  who  fractured  a  rib  on 
the  left  side,  some  three  weeks  prior  to  his  admission  to  my  wards 
for  pleuritic  effusion  on  the  injm-ed  side.  On  admission,  there 
was  dullness  and  absent  breath  sounds  up  to  the  third  rib  on 
the  left  side.     The  cardiac  dullness  reached  to  the  edge  of  the 


376 


DISPLACEMENT  OF  THE  HEART 


sternum,  showing  little  or  no  cardiac  displacement.  This  was 
not  to  be  wondered  at  in  a  man  of  fifty-eight,  whose  fibrous 
tissues  must  naturally  be  fairly  rigid.  Next  day,  60  ounces  of 
blood-stained  serum  were  removed  from  the  left  pleural  cavity, 
and  afterwards  it  was  found  that  the  left  lung  remained  rather 
dull  and  that  the  right  lung  crossed  over  to  the  left  of  the  sternum 

for    li-  inches    in   the  second 


I  inch  in  the 


left  space,  and 

third  space,  showing  some  dis- 
placement of  the  heart  towards 
the  affected  lung.  On  examin- 
ing the  lower  border  of  the 
right  lung  it  was  found  to 
be  displaced  downwards  (as 
shown  in  fig.  128),  as  was  also 
the  liver. 

Now  this  patient  gave  a 
history  of  having  had  no 
previous  illness;  but,  taking 
into  consideration  his  age  and 
the  probable  rigidity  of  his 
tissues,  it  was  not  credible 
that  a  pleurisy  with  effusion, 
lasting  at  most  two  or  three 
weeks,  could  have  caused  the 
displacement  of  his  heart  and 
liver  already  described.  Con- 
sequently, in  spite  of  his  state- 
ments to  the  contrary,  it  was 
certain  that  the  unexpanded  condition  of  the  left  lung  dated 
back  many  months,  if  not  years,  and  was  not  due  to  the 
traumatic  pleurisy  which  followed  the  accident. 

Careful  questioning  elicited  the  fact  that  he  had  been  rather 
short  of  breath  for  a  long  time,  and  brought  out  a  history 
pointing  to  a  very  long-standing  pleurisy  of  the  left  side.  Here 
the  careful  search  for  a  sUght  degree  of  cardiac  displacement 
led  to  the  making  of  a  correct  diagnosis.  The  evidence  given 
by  the  slight  displacement  of  the  heart  would  have  been  most 
important  if  an  action  for  damages  had  been  brought  by  the 
patient. 


Fig.  137. 

Displacement    of    Heart    to    tii 
Left  and  the  Liver  Downwards 


LATERAL  DISPLACEMENT 


377 


6.  Displacement  of  the  Heart  to  the  Eight. — Li  the 
cases  of  lateral  displacement  to  which  I  have  referred,  the  dis- 
placement of  the  heart  has  been  to  the  left,  but  precisely 
similar  help  in  diagnosis  can  be  obtained  where  the  disease  has 
involved  the  right  side,  except  for  the  fact  that  the  heart  does 
not  seem  quite  so  free  to  move  towards  the  right  side  as  towards 
the  left,  and  cases  of  displacement  to  the  right  seem  to  be  less 
frequent  than  those  to  the  left  (see  also  p.  381). 

Displacement  of  the  Heart  to  the  Right  by  Gradual  Collapse  of  the 

RiCHT  Lung 


6    spcbce 
in  A.A.L. 

mid.A. 


omAch 


Fig.  138. 

George  B.,  aged  thirty-five,  October .  20, 
1904.  Showing  displacement  due  to  fibrosis 
of  the  right  lung. 


Fig.  139. 

George  B.,  Jfarch  30,  190G.  Heart  more 
displaced  to  tlie  right.  Edge  of  left  lung 
2  inches  to  right  of  the  middle  line. 


The  following  is  an  extreme  case  of  displacement  of  the 
heart  to  the  right  : — 

G.  B.,  a  man  about  thirty-five,  was  seen  by  me  iirst  in 
October  1904.  He  was  suffering  from  phtliisis  involving  the 
right  lung  only.  There  was  such  marked  retraction  of  the 
diseased  lung  with  expansion  of  the  healthy  one  that  the  cardiac 
dullness  and  pulsation  was  displaced  to  the  right  of  the  sternum, 
and  the  resonance  of  the  left  lung  crossed  the  middle  line,  and 
during  ordinary  respiration  was  to  be  detected  nearly  1  inch  to 
the  right  of  the  sternum.  The  right  border  of  the  heart  was 
close  to  the  right  nipple  line  in  the  fourth  right  interspace,  as 
shown  in  fig.  138. 


378 


DISPLACEMENT  OF  THE  HEAKT 


Ed^e  of 
lunsr  ■' 
Fui       .  „ 
inspiration 

Full  expirv- 


During  the  next  two  years  extensive  fibrosis  took  place, 
greatly  reducing  the  size  of  the  right  lung  ipide,  fig.  139). 

By  ]\Iarch  1907,  the  remains  of  the  right  lung  occupied  but  a 
very  small  area  in  the  upper  and  posterior  part  of  the  axilla  and 
at  the  back. 

In  front,  the  full  resonance  of  the  right  lung  crossed  well  to 
the  right  of  the  sternum,  and  the  edge  of  this  lung  reached  to 
beyond  the  right  nipple  line  in  the  first  and  second  interspaces 
and  was  in  the  nipple  line  in  the  third  interspace. 

The  cardiac  dullness  and  pulsation  began  just  to  the  left 

of  the  sternum  in  the  fourth 
interspace  and  extended  to 
nearly  the  mid-axillary  line 
{pide  fig.  140). 

Posteriorly,    the    left   lung 
crossed   over   the   middle    line 


Vosition_af. 
traches; 


to  the    extent  of  some    \\  or 
2  inches. 

This  man  died  in  March 
1907  from  amyloid  disease  of 
the  kidneys,  and  the  post- 
mortem examination  con- 
firmed the  clinical  observations 
as  to  the  position  of  the  heart 
and  the  extremely  contracted 
state  of  the  right  lung.  It  was 
little  more  than  the  size  of  the 
hand  and  some  \\  or  2  inches 
thick,  and  consisted  simply  of 
fibrous  tissue  and  dilated 
bronchial  tubes  or  healed  tubercular  cavities. 

The  heart  lay  on  the  right  side,  but  most  unfortunately  I  was 
not  present  at  the  post-mortem ;  and  in  spite  of  the  unusual 
nature  of  the  case  no  notes  were  recorded  as  to  the  relative 
positions  occupied  by  the  various  parts  of  the  heart. 


Fig,  140. 

George  B.,  March  1907.  Heart  in  right 
axilla.  Edge  of  left  lung  crosses  over  the 
right  nipple  line. 


In  spite  of  this  extreme  displacement,  the  only  murmur 
present  was  a  moderately  loud  and  locaHsed  sj^stolic  murmur 
audible  about  the  right  nipple  line  in  the  fom'th  and  fifth 
interspaces. 

Before  leaving  this  subject,  I  will  briet'y  refer  to  a  case 
illustrating  a  somewhat  less  frequent  cause  of  displacement. 


ITS  ALTERED  RELATIONSHIPS  379 

The  patient  was  an  old  man  suffering  from  bronchitic  symp- 
toms. Examination  of  his  chest  showed  the  fact  that  his  heart 
was  much  displaced  to  the  right,  and  its  right  limit  of  pulsation 
was  in  the  right  nipple  line.  The  action  of  the  upper  part  of 
the  right  lung  was  very  defective,  and  it  was  evident  that  there 
was  a  considerable  amount  of  fibrosis  of  it.  This  shrinking  of 
the  right  lung,  coupled  with  the  compensatory  enlargement  of 
the  left  lung,  was  the  cause  of  the  displacement  of  the  heart. 
The  fibrosis  of  the  right  lung  was  due  to  the  infiltration  of  the 
root  of  the  lung  by  a  malignant  tumour. 

The  man  lived  some  months,  and  before  his  death  the  tumour 
had  increased  so  much  in  size  that  its  growth  more  than  made 
up  for  the  destruction  of  the  lung,  and  the  heart  was  pushed 
back  into  its  normal  position.  This  was  verified  at  the  post- 
mortem examination. 


Altered  Relationships  op  the  Heart  when  Displaced 

When  the  heart  is  pushed  or  drawn  out  of  its  normal  position, 
there  is  often  a  certain  amount  of  rotation  also,  and  I 
propose  in  conclusion  briefly  to  discuss  this  subject. 

The  fact  that  the  heart  rotates  when  moved  in  certain 
directions  shows  that  certain  of  its  attachments  are  more  fixed 
than  others,  and  it  will  help  the  consideration  of  the  subject  to 
summarise  briefly  its  points  of  attachment  and  their  relative 
fixity. 

Generally  speaking,  the  ventricles  of  the  heart  are  most 
free  to  move,  and  the  auricles  the  most  fixed.  But  to  under- 
stand the  changes  which  take  place,  a  more  detailed  view  is 
necessary. 

The  right  amicle  is  fixed  to  the  diaphragm  hj  the  inferior 
cava. 

The  right  auricle  is  fixed  to  the  deep  fascia  of  the  neck,  and 
the  root  of  the  lung  by  the  superior  cava,  &c. 

The  left  auricle  is  fixed  to  the  root  of  the  lungs  hj  the 
pulmonary  veins. 

The  upper  anterior  part  of  the  right  ventricle  is  fixed  to  the 
anterior  part  of  the  root  of  the  left  lung  by  the  left  branch  of 
the  pulmonary  artery. 

The  upper  anterior  part  of  the  right  ventiicle  is  fixed  to 


380  DISPLACEMENT  OF  THE  HEAKT 

the  posterior  part  of  the  root  of  the  right  hing  by  the  right 
branch  of  the  pulmonary  artery. 

The  upper  central  part  of  the  base  of  the  heart  is  fixed  to 
the  fascia  of  neck,  &c.,  by  the  aorta. 

Of  these,  the  attachments  of  the  aorta  and  superior  vona 
cava  are  farthest  from  the  heart  and  of  less  value  than  the 
others  in  preventing,  or  interfering  with,  cardiac  displace- 
ment. 

The  attachments  to  the  root  of  either  lung  are,  on  the 
other  hand,  short,  and  will  greatly  tend  to  hinder  displacement 
of  the  organ,  'provided  that  the  roots  of  the  lungs  are  not 
themselves  tending  to  move. 

Now  the  attachment  of  the  right  auricle  to  the  diaphragm 
by  means  of  the  inferior  cava  is  the  shortest  of  all  the  above- 
mentioned  points  of  attachment,  and  the  fibrous  portion  of 
the  diaphragm  to  which  it  is  attached  is  also,  except  for  the 
normal  range  of  upward  and  downward  movement  decidedly 
a  fixed  point.  I  believe  this  point,  where  the  right  auricle 
is  practically  fixed  to  the  diaphragm,  is  to  be  regarded  as  the 
pivot  around  which  the  heart  turns  in  the  various  displacements 
to  which  it  is  subject.  In  the  lesser  degi'ees  of  displacement,  the 
fixation  of  the  left  auricle  (which  lies  posteriorlj^)  to  the  roots 
of  the  two  lungs,  is  also  a  fixed  point,  so  long  as  the  roots  of 
the  lungs  themselves  remain  fixed.  In  the  extreme  cases, 
however,  where  collapse  of  one  or  other  lung  is  accompanied 
by  great  increase  in  size  of  the  other,  there  is  good  reason  to 
believe  that  the  median  position  of  the  root  of  the  lungs  does 
not  remain  unchanged,  but  that  the  structures  of  the  posterior 
mediastinum  are  moved  over  en  masse  by  the  shrinkage  of 
the  one  lung  and  the  increase  in  size  of  the  other. 

When  this  movement  of  the  whole  mediastinum  takes 
place — as  it  seems  to  do  very  frequently  in  these  cases — much 
rotation  of  the  heart  will  not  take  place,  and  the  only  attach- 
ment likely  to  cause  any  alteration  in  the  relative  position 
of  its  chambers  "will  be  the  fixation  of  the  inferior  cava 
to  the  diaphragm  in  cases  where  the  heart  is  shifted  to  the 
right. 

In  any  well-marked  case  it  is  easy  to  demonstrate  the 
movement  of  the  mediastinal  tissues  by  noting  the  situation 


ITS  ALTERED  RELATIONSHIPS  381 

in  wliich  ilio  lower  cud  of  the  trachea  eiileis  Iho  thorax.  It 
is  not  uncommon  to  lind  it  wholly  to  the  right  or  left  of  the 
middle  hne,  and  in  the  case  illustrated  by  fig.  140  the  left  side 
of  the  trachea  was  under  the  left  border  of  the  right-  sterno- 
mastoid. 

A  similar  amount  of  displacement  may  also  be  seen  on  the 
left  side. 

This  movement  of  the  root  of  the  lung  is  also  suggested 
by  the  way  in  wliich  the  resonance  of  one  lung  will  cross  over 
the  middle  hne  posteriorly. 

Over  the  lower  part  of  the  chest,  where  we  often  lind 
the  crossing  over  from  one  side  to  the  other  of  dullness  due 
to  fluid,  or  of  resonance  due  to  compensatory  enlargement, 
this  crossing  over  has  not  the  same  significance,  as  it  is  simply 
due  to  the  displacement  of  the  membranous  division  between 
the  two  halves  of  the  thorax  when  the  pressure  on  one  side 
exceeds  that  on  the  other.-^  '  It  is,  how^ever,  a  phenomenon 
of  very  great  diagnostic  value. 

With  regard  to  the  presence  of  rotation  of  the  heart  on 
itself  when  displaced  upwards  or  downw^ards,  there  does  not 
seem  to  be  any  reason  to  expect  that  such  should  occur,  nor  is 
there  any  clinical  evidence  of  such  rotation. 

In  displacement  to  the  right,  however,  the  case  is  different, 
and  the  changes  the  heart  undergoes  seem  somewhat  com- 
plicated. The  follomng  is  a  summary  of  a  case  illustrating 
this  :— 

T.  F.,  aged  forty-three,  suffering  from  bronchitic  symptoms. 
Physical  examination  of  the  chest  showed  that  there  was  very 
considerable  fibrosis  of  the  right  lower  lobe,  with  some  excava- 
tion. The  upper  part  of  the  right  lung  and  the  whole  of  the  left 
were  health3^  The  heart  was  drawn  over  to  the  right,  and  the 
cardiac  dullness  and  pulsation  were  mainly  to  the  right  of  the 
sternum.  The  cardiac  and  hepatic  dullness  w^ere  as  shown  in 
the  diagram  (fig.  141). 

An  auricle  w^as  pulsating  in  the  right  nipple  line  (over  the 
area  which  is  dotted  in  fig.  141),  and  this  must  have  been  the 
right  auricle.     There  was  ventricular  pulsation  above  and  to 

1  Where  dullness  duo  to  pleuritic  efEusion  crosses  over,  this  area  is 
sometimes  called  '  Grccco's  triangle.' 


382 


DISPLACEMENT  OF  THE  HEART 


the  left  of  this  area,  as  far  as  the  third  interspace  midway  to  the 
right  nipple  line.  Over  the  upper  part  of  this  area  the  second 
sound  was  well  heard,  and  its  area  of  maximum  loudness  was 
in  the  third  and  fourth  right  interspaces,  as  shown  in  fig.  132. 
This  must  have  been  the  right  ventricle,  and  the  area  of  maxi- 
mal loudness  of  the  second  sound  showed  the  situation  of  its 
conus  arteriosus  and  the  origin  of  the  pulmonar}^  artery  to  be 

some  2  to  3  inches  to  the 
right  of  the  usual  position. 
There  was  a  little  cardiac 
dullness  to  the  left  of  the 
sternum  in  the  fourth  and 
fifth  interspaces,  with  faint 
pulsation  and  almost  in- 
audible heart  sounds.  This 
meant  that  the  left  ventricle 
was  not  as  near  the  chest 
wall  as  normal. 


The  explanation  of  this 
condition  is  as  follows,  and 
it  is  a  type  of  what  may  be 
expected  in  displacement  of 
the  heart  to  the  right  by 
shrinking  of  the  lower  part 
of  the  right  lung  : — 

The  traction  of  the  con- 
tracted lung  takes  place 
pulmonary    artery   and  vein 


Fig.  141. 
Displacement  of  Heakt  to  the  Right. 

Dotted  area  =  auricular  pulsation. 
X  =  area  of  maximum  loudness  of  second  sound. 


through  the   branches    of    the 
which  go  to  the  affected  lung. 

Now  the  right  branch  of  the  pulmonary  artery  takes  origin 
from  the  front  of  the  heart,  but  passes  behind  the  aorta  to  get 
to  the  right  lung.  Traction  in  this  artery  ^nU  therefore  tend 
to  rotate  the  heart  about  an  axis  running  through  the  two 
relatively  fixed  points — namely,  the  aorta  and  the  base  of  the 
right  auricle  where  the  inferior  vena  cava  passes  through  the 
diaphragm.  This  rotation  would  bring  the  right  border  of  the 
rio;ht  auricle  forwards  into  closer  contact  with  the  chest,  and 
make  the  left  ventricle  and  the  apex  of  the  heart  recede  fi'om 
the  chest  wall  just  as  was  shown  to  be  the  case  by  the  physical 
examination  of  the  patient. 


ITS  ALTERED  KELATIONSHIPS  383 

A  similar  effect  will  be  produced  by  the  traction  on  the 
pulmonary  veins,  ruimingas  they  do  from  the  diseased  lung  to 
the  left  auricle  posteriorly. 

As  regards  the  displacement  of  the  heart  to  the  left  by 
retraction  of  the  left  lung.  In  this  case  there  is  but  Httle 
rotation,  as  the  vessels  pulled  upon  arise  from  the  left  side  of 
the  heart,  and  the  fixed  points  are  on  the  opposite  side. 

There  is,  however,  sometimes  a  slight  degree  of  rotation, 
and  the  left  ventricle  and  auricle  come  to  lie  rather  more 
anterior,  and  the  right  auricle  more  posterior,  than  would 
be  the  case  were  the  heart  simply  pushed  over  as  a  whole. 

As  to  the  presence  of  murnmrs.  This  is  a  somewdiat 
comphcated  question,  and  one  that  is  by  no  means  settled 
at  the  present  day.  I  am  glad,  however,  to  be  able  to  make 
a  clear  statement  on  the  subject — namely,  that  it  is  possible 
to  have  the  most  extreme  degrees  of  displacement,  either  to 
the  right  or  to  the  left,  without  any  murmurs  at  all.  This  also 
holds  true  of  the  displacement  which  accompanies  dilatation  of 
the  right  ventricle,  as  described  on  p.  360,  for  in  this  case  there 
was  an  entire  absence  of  murmurs.  If,  however,  these  same 
displacements  occur  in  ansemic  individuals,  there  may  be 
extremely  loud  murmurs,  into  which  I  cannot  go  in  this  paper. 
There  is  certainly  no  characteristic  murmm*  in  these  cases, 
and  I  have  often,  I  must  confess,  felt  surprised  at  the  absence 
of  murmurs  in  cases  of  extreme  cardiac  displacement. 

This  absence  of  murmurs,  even  in  extreme  cases  of  displace- 
ment, shows  that  the  attachments  of  the  heart  to  the  chest 
wall  are  nowhere  rigid  enough,  as  a  rule,  to  produce  kinking  or 
compression  of  the  large  vessels,  such  as  would  be  the  case  were, 
for  instance,  the  roots  of  the  lungs  immovably  fixed  Lu  the  spine. 

It  also  helps  to  explain  the  slightness  of  the  cardiac  symp- 
toms which  are  noticeable  in  a  simple  case  of  cardiac  displace- 
ment, even  when  extreme  in  degree — more  especially  when  such 
displacement  is  towards  the  left.  In  fact,  the  heart  seems 
capable  of  doing  its  work  as  easily  when  lying  in  the  left  axilla 
as  when  it  is  in  its  normal  situation. 

I  cannot,  therefore,  say  that  there  are  any  special  symptoms 
characteristic  of  cardiac  displacement,  or  that  any  special 
treatment  is  necessary. 


PART  III.— ESSAYS  DEALING  WITH  VALVULAR 
DISEASE,  ESPECIALLY  IN  RELATION  TO 
VENTRICULAR  EXPANSION. 

Essay  IX.— ON  THE  NATUEE  OF  THE  EXPANSION 
PHASE  OF  THE  CAEDIAC  CYCLE  AND  THE 
PHENOMENA  ASSOCIATED  WITH  IT^ 

[This  essay  is  mainly  a  summary  of  what  is  brought 
forward  in  the  three  foUowing  essays  with  regard  to  the 
muscular  expansion  of  the  ventricles.] 

The  object  of  this  paper  is  to  advocate  the  view  that  the 
ventricles  of  the  heart  are  filled  by  their  own  muscular  action 
and  not  by  the  auricular  contraction,  and  to  show  how  this 
theory  suffices  to  explain  the  various  phenomena  observable 
in  valvular  disease  of  the  heart. 

It  is  more  than  twenty  years  since  dissatisfaction  was 
openly  expressed  with  the  old  theory  as  to  the  forces  which 
fill  the  ventricles,  and  the  belief  has  since  been  gaining  ground 
that  the  muscular  fibres  of  the  heart  are  able,  not  only  to 
develop  force  by  their  longitudinal  contraction,  but  also,  by  an 
act  of  longitudinal  muscular  expansion,^  to  enlarge  the  cavity 
of  the  heart  so  as  to  develop  force  in  the  reverse  direction. 
In  other  words,  the  behef  is  surel}''  gaining  ground  that 
the  heart  is  a  double-acting  pump,  filhng  its  chambers  by  its 
own  back  stroke,  and  that  the  ventricles  are  not  dependent 
upon  the  auricles,  or  other  outside  agency,  so  ftir  as  the 
reception  of  the  main  part  of  their  charge  is  concerned. 

It  is,  after  all,  only  natm'al  to  beheve  that  such  a  perfect 
pump  as  the  heart  is,  should  not  be  inferior,  in  its  mechanism, 
to  the  pumps  which  the  wit  of  man  devises. 

It  was  twenty-four  years  ago  that  this  theory  was  first 
brought  under  my  notice  by  Dr.  Lockhart  Gibson,  then  of 
Edinburgh  and  now  of  Brisbane,  who  pointed  out  the  support 

^  See  The,  Praclilioner  for  November  1907. 
Due  probably  to  transverse  contraction,  according  to  Sir  Lauder  Brunton. 

384 


EXPANSION  PHASE  OF  CAKDIAC  CYCLE     [|    385 

which  the  experiments  of  the  late  Professor  Rutherford  gave 
to  this  view,  by  his  demonstration  that  after  receiving  a 
minimal  galvanic  stimulus,  a  striped  muscular  fibre  would, 
after  contraction,  suddenly  return  towards  its  former  length, 
and  that  the  force,  developed  by  this  sudden  expansion,  was 
approximately  two-fifths  of  that  developed  during  contraction. 

If  these  observations  of  Professor  Rutherford  had  been 
generally  accepted,  the  theory  of  the  expansion  of  the  heart 
muscle  would  have  rested  on  a  sure  basis.  There  seems, 
however,  to  be  some  doubt  as  to  the  true  interpretation  of 
his  experiments,  and,  therefore,  in  the  absence  of  a  physio- 
logical basis  (apart  from  the  fact  that  a  transient  negative 
phase  is  demonstrable  in  the  intraventricular  pressure  curve), 
we  have  to  depend  upon  chnical  evidence.  Clinical  evidence  is, 
however,  not  easy  to  obtain,  owing  to  the  nature  of  the  problem. 

]\Iuch  can  be  done  l)y  the  careful  study  of  the  heart's 
movements  in  health  and  disease  by  means  of  the  cardio- 
graph, but  the  time  required  to  make  careful  observations, 
and  then  to  measure  and  correlate  the  tracings,  is  very  great, 
for  very  many  tracings  must  be  taken  from  all  possible  parts 
of  the  cardiac  area,  and  from  the  large  arteries  and  veins, 
before  the  interpretation  of  the  cardiograms  is  possible  with 
any  degree  of  certainty. 

As  a  result  of  very  numerous  observations  during  the  last 
sixteen  years,  I  am  certain  that  the  cardiograph  shows  con- 
clusively that  the  phase  of  ventricular  contraction  is  followed 
by  an  active  expansion  movement. 

Cardiographic  Evidence 

1.  As  is  well  Imown,  the  cardiac  muscle  does  not  at  once 
relax  after  the  closure  of  the  semilunar  valves,  and,  if  the  time 
of  occurrence  of  the  second  sound  is  carefully  recorded  on  the 
cardiogram  by  an  electric  signal,  this  can  be  clearly  demon- 
strated in  tracings,  taken  at  the  apex  or  over  the  centre  of 
the  heart.  Thus  the  cardiograph  shows  that  the  heart  muscle 
remains  liard,  and  therefore  active,  for  an  appreciable  time  after 
the  end  of  the  systole,  and  relaxation  does  not  immediately 
follow  the  end  of  the  systole  as  marked,  by  the  closure  of 
the  semilunar  valves.^ 

»  Essay  X,  p.  403. 

2  c 


386  EXPANSION  PHASE  OF  CARDIAC  CYCLE 

2.  Further,  the  cardiograph  shows  quite  clearly  that,  during 
this  post-systolic  activity,  the  heart  muscle  does  not  remain 
contracted,  for  the  size  of  the  ventricle  is  rapidly  increasing. 
This  can  be  demonstrated,  if  a  series  of  tracings  is  taken  from 
one  side  of  the  central  axis  of  an  enlarged  heart,  where  many 
different  tracings  are  obtainable.  Such  tracings  clearly  show  a 
fall,  due  to  the  diminution  in  the  size  of  the  ventricle  as  the 
blood  is  expelled  from  it ;  and  following  this  fall  is  a  sudden 
rise,  pointing  to  the  sudden  return  of  the  ventricle  towards  the 
size  it  was  at  the  commencement  of  systole. 

A  record  of  the  time  of  occurrence  of  the  second  sound, 
upon  this  type  of  cardiogram,  shows  that  the  maximal 
diastolic  rise  takes  place  immediately  after  the  occurrence  of 
the  second  sound  of  the  heart. 

I  do  not  here  refer  to  ordinary  inverted  tracings — because 
these,  when  they  are  not  due  to  faulty  manipulation,  are  not 
very  trustworthy — but  to  the  cardiograms  showing  a  systolic 
rise,  and  then  a  fall  followed  by  another  rise  {vide  Plates 
VII  and  XII). 

The  fact  that  this  diastolic  increase  in  the  size  of  the  heart 
has  power  to  hft  the  lever  of  the  cardiograph  against  a  pressure 
of  some  two  or  three  ounces,  or  more,  shows  that  it  cannot  be 
merely  due  to  the  elastic  recoil  of  the  relaxed  muscle,  neither 
can  it  be  due,  as  has  been  suggested,  to  the  inrush  of  the  blood, 
which  has  accumulated  in  the  auricle  during  the  time  of 
closure  of  the  mitral  valve.  The  mitral  valve  only  remains 
closed  for  less  than  half  of  the  cardiac  cycle,  the  auricle  cannot, 
therefore,  be  much  more  than  half  full  when  the  mitral  valve 
opens,  and  there  can  therefore  be  no  inrush  of  blood  under 
pressure  from  the  auricle  into  the  ventricle  at  this  point  of  the 
cardiac  cycle.  Study  of  the  cardiogram  in  dilatation  of  the 
ventricle  hence  appears  to  prove  that  true  muscular  expansion 
follows  muscular  contraction. 


Expansion  Phase  of  the  Cardiac  Cycle 

This  period  of  expansion  of  the  muscular  fibres  appears 
to  be  a  definite  and  well-defined  phase  of  the  cardiac  cycle. 
Both   cardiographically   and    clinically,   its   duration   is   well 


EXPANSION  PHASE  OF  CARDIAC  CYCLE  387 

defined,  and  careful  measurements  of  the  portion  of  the  cardio- 
gram representing  this  phase,  as  well  as  measui'ements  of 
records  of  the  cardiac  sounds  which  mark  its  duration,  show 
its  length  to  be  about  one-tenth  of  a  second.  Moreover,  its 
length  does  not  seem  to  vary,  as  do  the  other  phases  of  the 
cardiac  cycle ;  but,  whether  the  heart  is  beating  slowly  or 
rapidly,  it  still  has  a  duration  of  one-tenth  of  a  second.^ 

We  must,  therefore,  alter  om'  conception  of  the  cardiac 
cycle,  and  insert  in  it  a  phase  of  expansion,  thus  : — 

Ventricular  contraction  lasting  -j^  of  a  second, 
expansion         „      ^ 
,,  relaxation        ,,      "ttt      >j      >> 

The  Function  of  the  Auricles 

This  being  so,  certain  other  points  arise  in  connection  with 
the  function  of  the  am-icles. 

If  the  size  of  the  mitral  orifice  is  noted  in  relation  to  the  cubic 
content  of  the  left  auricle,  it  must,  I  think,  be  acknowledged 
that,  under  powerful  suction,  the  contents  of  this  chamber 
would  be  immediately  drawn  into  the  ventricle,  although  the 
aspiration  lasted  only  one-tenth  of  a  second,  and  that  there- 
fore the  auricle  would  be  empty  by  the  time  relaxation  of 
the  ventricle  set  in.  According  to  the  old  theory,  the  auricle 
also  empties  itself  dm'ing  its  systole.  If  this  were  so,  the 
auricle  would  be  twice  emptied  in  each  cycle. 

Now,  during  any  particular  cycle,  as  the  flow  of  blood  from 
the  pulmonary  arteries  into  the  auricle  is  more  or  less  regular, 
this  double  emptying  of  the  amicle  should  result  in  its  never 
having  to  hold  the  full  charge  of  blood.  In  other  words,  if 
the  heart  throws  3  ounces  of  blood  with  each  beat,  we  should 
expect  to  find  that  the  cubic  content  of  the  normal  auricle 
was  somewhere  about  half  of  this  amount. 

But,  as  the  normal  capacity  of  the  auricle  is  at  least 
3  ounces,  there  must  be  some  error  in  this  supposition.  The 
error  lies,  I  believe,  in  supposing  that  there  is  any  considerable 
general  emptying  of  the  auricle  during  the  auricular  systole. 

'  Essay  XII,   p.  429. 


388  EXPANSION  PHASE  OF  CARDIAC  CYCLE 

It  is  probable,  as  was  suggested  by  Mayo  Collier,^  in  1889,  that 
the  function  of  the  auricle  is  only  to  throw  a  small  quantity 
of  blood  into  a  nearly  full  ventricle,  by  means  of  the  highly 
muscular  appendix,  for  the  purpose  of  closing  and  stretching 
the  auriculo-ventricular  valves  prior  to  the  commencement 
of  systole  ;  and  that  the  body  of  the  auricle  has  little,  if  any, 
power  of  emptying  itself  by  its  own  contraction.  This 
function,  therefore,  of  the  body  of  the  auricle  is  to  act  as  a 
reservoir,  rather  than  as  an  accessory  force-pump  for  filling 
the  ventricle,  and  the  function  of  its  muscular  fibres  is  simply 
to  make  its  walls  tense  enough  for  the  action  of  the  appendix 
to  take  place  {vide  p.  529). 

This  view  of  the  function  of  the  auricles  fits  in  very  well 
with  the  demands  of  the  theory  which  we  are  discussing. 

If  the  auricle  does  not  empty  itself  to  any  extent  at  the 
time  of  the  auricular  systole,  and  is  only  emptied  by  the 
aspiration  of  the  ventricle,  it  follows  that  that  aspiration 
must  draw  into  the  ventricle  the  greater  part  of  its  full 
charge  of  blood — namely,  nearly  3  ounces.  [If  this  is  so,  it 
is  possible  that,  under  certain  circumstances,  the  reception  of 
this  full  charge  may  cause  a  preliminary  closure  of  the  tricuspid 
or  mitral  valve  by  its  tendency  to  escape  back  into  the  auricle, 
and  that  the  faint  sound,  which  is  sometimes  heard  at  the  com- 
mencement of  the  phase  of  relaxation,  and  which  I  call  the 
third  sound  of  the  heart,  may  sometimes  be  caused  by  this 
quiet  closure  of  these  valves.^] 

We  may,  I  think,  assume  that  the  body  of  the  auricle  acts 
simply  as  a  reservoir,  in  which  blood  collects,  and  thus  enables 
what  is  practically  a  full  charge  of  3  ounces  to  be  drawn  into 
the  ventricle  during  its  expansion  phase. 

Clinical  Evidence  as  to  the  Nature  of  the  Expansion 

Movement 

It  is  not  easy  to  obtain  direct  clinical  evidence  as  to  the 
nature  of  the  expansion  movement,  but  such  evidence  as  is 

1  The  Physiology  of  the  Vascular  System,  p.  10. 

2  It  is  more  probable  that  the  tonic  contraction  of  the  auricle  and  great 
veins  suffices  to  keep^the  blood  in  the  relaxed  ventricle. 


EXPANSION  PHASE^OF  CARDIAC  CYCLE  389 

obtainable  is  all  in  favoui-  of  this  theory,  for  by  it  all  the  pheno- 
mena of  valvular  disease  can  be  explained  very  much  more 
satisfactorily  than  by  the  older  theory. 

As  to  mitral  regurgitation  and  stenosis  : 

According  to  the  accepted  theory,  when  compensation  fails 
in  mitral  disease,  extra  work  is  thrown  upon  the  right  ventricle 
by  the  delay  in  the  pulmonary  circulation,  and  the  re-estabUsh- 
ment  and  maintenance  of  compensation  depend  upon  the  success, 
or  otherwise,  of  the  efforts  of  the  right  ventricle  to  overcome 
this. 

When  the  power  of  the  ventricular  expansion  is  reahsed, 
this  statement  must  be  modified,  so  far  as  the  jnaintenance 
of  compensation  is  concerned,  for  this  must  depend  upon  the 
success  of  the  left  ventricle  in  compensating  for  its  own  defects. 
If  the  left  ventricle  fails,  then,  and  then  only,  is  extra  work 
thrown  upon  the  right  ventricle,  and  its  assistance  called  for. 

Mitral  Regurgitation 

Adequate  compensation  for  mitral  regurgitation  must 
consist  in  both  dilatation  of  the  ventricular  cavity,  and  hyper- 
trophy of  its  walls  (see  Davies's  '  Circulation  through  Diseased 
Hearts,'  1887),  i.e.  dilatation  enough  to  enable  the  heart  to 
hold  the  normal  charge,  'plus  the  amount  which  will  regurgitate 
into  the  auricle  and  hypertrophj,  so  that  it  may  have  strength 
to  throw  this  extra  amount. 

Now,  according  to  the  theory  mider  discussion,  this  change 
in  the  heart  will  not  only  suffice,  so  far  as  the  sj'stolic  work  of 
the  ventricle  is  concerned,  but  will  also  give  the  extra  power 
necessary  properly  to  fill  the  ventricle  during  diastole.  For 
this  increase,  both  in  its  cubic  content  and  strength,  will 
increase  its  capability  of  aspirating  blood  from  the  auricle, 
and  to  the  extent  rendered  necessary  by  the  amount  of  the 
leakage.  Therefore,  at  the  end  of  the  expansion  movement 
in  compensated  mitral  regurgitation,  the  auricle  will  be  as 
fully  emptied  as  normal,  and  the  pulmonary  circulation  and 
the  right  side  of  the  heart  will  not  be  hampered. 

In  proof  of  this,  I  have  measured  the  loudness  of  the  pulmo- 
nary second  sound  in  cases  of  compensated  mitral  regurgitation, 


390  EXPANSION  PHASE  OF  CAKDIAC  CYCLE 

and  I  find  that  the  true  loudness  of  this  sound  does  not  exceed 
the  normal  limits,  thus  pointing  to  the  probabiUty  that  the 
right  ventricle,  in  such  cases,  is  not  ordinarily  called  on  to  do 
more  work  than  normal.^ 

There  is  usually  some  apparent  accentuation  of  this  sound 
in  these  cases,  but  this  is  due  to  the  sound  being  simply  sharper 
in  tone,  probably  owing  to  the  right  ventricle  increasing  the 
force  of  its  beat,  in  harmony  with  the  action  of  the  left,  and  it 
does  not  suggest  any  excess  of  pressure  in  the  pulmonary  artery 
as  will  be  explained  more  fully  later  on,  under  mitral  stenosis. 

Mitral  Stenosis 

It  is  from  mitral  stenosis  that  the  expansion  theory  receives 
the  most  clinical  support,  for  it  here  sweeps  away  the  diffi- 
culties which  used  to  surround  the  explanations  of  the  clinical 
phenomena  associated  with  this  condition. 

Process  of  Compensation 

In  order  to  overcome  the  hindrance  to  the  entrance  of 
blood  into  the  ventricle,  greater  aspiratory  force  is  needed. 
This,  according  to  the  theory  we  are  discussing,  could  be 
attained  by  the  ventricle  altering  its  beat. 

In  order  to  develop  the  maximal  amount  of  suction  dming 
the  short  expansion  period,  the  force  of  the  ventricular  con- 
traction w^ould  have  to  be  concentrated  upon  the  very  end  of 
the  systole  so  as  to  call  forth  the  greatest  possible  amount  of 
elastic  and  muscular  recoil  from  the  ventricular  Avail.  But  this 
change  in  the  character  of  the  beat  is  observable  in  mitral 
stenosis,  for  the  first  sound  is  abnormally  loud,  and  also  it 
ends  very  sharply,  just  as  might  be  expected  if  it  were  trying 
to  increase  its  suction  power.  I  have  heard  the  first  sound  of 
the  heart  2  feet  away  from  the  patient,  in  a  case  of  mitral 
stenosis,  whereas  normally  it  cannot  be  heard  with  a  binaural 
stethoscope  ^  inch  away  from  the  chest  wall.  Further 
evidence  on  this  point  is  given  by  the  fact  that,  where 
the  heart  in  mitral  stenosis  is  temporarily  embarrassed,  the 

•  Essay  XI,  p.  423. 


EXPANSION  PHASE  OF  CARDIAC  CYCLE  391 

loudness  of  the  first  sound  is  often  very  noticeably  increased 
for  a  time,  and  far  in  excess  of  the  increase  noticed  in  similar 
circumstances  in  health,  or  in  other  forms  of  heart  failure. 
In  such  a  case,  the  first  sound  returns  to  its  usual  loudness 
as  the  heart  recovers  itself.^ 

This  change  in  the  character  of  the  first  sound  is,  therefore, 
evidence  in  favour  of  the  expansion  theory,  though  it  does 
not  give  special  support  to  the  theory  of  muscular,  as  apart 
from  elastic,  expansion. 

Again,  the  fact  that  compensation  depends  upon  the 
muscular  action  of  the  left  ventricle  accounts  for  the  hyper- 
trophy which  is  often  noticeable  in  mitral  stenosis,  and  which, 
according  to  the  older  theory,  would  not  be  so  easily  explained  ; 
also,  in  cases  of  death  in  mitral  stenosis  without  rupture  of 
compensation,  it  has  been  noticed  that  the  left  auricle  is  of 
normal  size,  and  not  dilated.  This  is  what  would  be  expected, 
if  compensation  were  wholly  due  to  the  increased  suction 
power  of  the  ventricle,  but  would  be  very  hard  to  account 
for  by  the  older  theory  of  compensation. 

Pulmonary  Second  Sound  in  Mitral  Stenosis 

This  theory  of  the  freedom  of  the  amicle  from  any 
embarrassment,  in  cases  of  well-compensated  mitral  stenosis, 
is  fmther  emphasised  by  the  character  of  the  pulmonary 
second  sound,  for,  in  the  majority  of  these  cases,  which  I 
have  carefully  measm-ed,  it  does  not  exceed  the  normal  hmit 
of  loudness,  and  in  some  cases  is  well  within  that  limit.  This 
statement  may  appear  to  conflict  with  what  is  a  weU-recognised 
sign  of  mitral  stenosis — namely,  accentuation  of  the  pulmonary 
second  sound,  but  it  does  not  really  do  so.  In  most  of  these 
cases,  the  second  sound,  when  heard  by  the  stethoscope, 
ap'pears  to  be  much  louder  than  normal ;  but,  if  some  means  are 
taken  of  deadening  the  sound,  it  vnR  be  found  that  its  pene- 
trative power  is  not  increased,  showing  that  there  is  no  increase 
in  the  volume  of  the  sound,  as  would  be  the  case  if  it  were 
due  to  increased  tension  in  the  pulmonary  artery.  This 
can  be  easily  demonstrated  by  inserting  a  deflated  rubber  toy 

1  Essay  XI,  p.  425. 


392  EXPANSION  PHASE  OF  CAKDIAC  CYCLfi 

balloon  under  the  stethoscope,  and  slowly  Hfting  it  by  inflating 
the  balloon  through  a  tube  with  the  mouth.  So  long  as  the 
stethoscope  is  within  |  or  f  of  an  inch  of  the  chest  wall,  the 
sound  retains  its  loudness;  but,  when  the  stethoscope  is  raised 
higher,  the  sound  is  rapidly  damped  down,  and  is  extinguished 
at  1  inch  or  1|  inches,  as  is  the  case  with  a  normal  second 
sound.  In  uncompensated  mitral  stenosis,  on  the  other 
hand,  where  the  right  ventricle  is  doing  extra  work,  the 
sound  may  often  be  heard  as  far  away  as  If  or  1|  inches 
or  more. 

In  other  conditions,  where  the  right  side  of  the  heart  is 
doing  extra  work,  true  increase  in  the  loudness  of  the  pul- 
monary  second  sound  may  also  be  observed.  For  instance, 
in  some  cases  of  ansemia,  in  which  the  tension  in  the  pul- 
monary artery  is  certainly  increased,  the  second  sound  may 
be  heard  when  the  stethoscope  is  raised  as  much  as  2|  inches 
from  the  chest  wall  instead  of  the  normal  1|  inches,  and,  in 
such  a  case,  the  sound  may  even  be  audible,  without  the 
interposition  of  the  rubber  bag,  with  the  stethoscope  |  or  J 
inch  from  the  chest  wall.  Such  a  degi'ee  of  accentuation  as 
this  I  have  never  seen  in  fully  compensated  mitral  stenosis 
or  regurgitation,  although  it  surely  ought  to  occur  if  the 
maintenance  of  compensation  really  depended  upon  the  work 
of  the  right  heart.  I  have  not  infrequently  noted  an  accentua- 
tion nearly  as  great  as  this  occurring  during  the  process  of 
compensation,  but  which  materially  lessened  as  compensation 
became  more  perfect. 

Spurious  Accentuation  of  the  Second  Sound 

The  explanation  of  the  apparent  loudness  of  the  pulmonary 
Second  sound,  in  these  cases  of  compensated  mitral  disease,  is 
to  be  found  in  the  fact  that  the  right  ventricle  cannot  but 
partake  in  the  forcible  action  of  the  left  ventricle,  and  the 
increase  of  suction,  which  results  therefrom,  causes  the  blood 
in  the  pulmonary  artery  to  return  with  gi-eater  rapidity  against 
the  pulmonary  valves;  but,  as  there  is  only  the  normal  volume 
of  blood  in  the  artery,  although  the  sharimess  of  the  sound 
may  be  increased,   its   volume  is  not.     It   is  the   difference 


EXPANSION  PHASE  OE  CARDIAC  CYCLE  393 

between  the  sound  of  a  sharp  blow  with  a  small  hammer  and 
the  more  penetrating  sound  of  a  less  sharp  blow  with  a  heavier 
hammer. 

This  absence  of  a  true  accentuation  of  the  pulmonary 
second  sound  in  mitral  stenosis  is  therefore  evidence  that 
the  increased  ventricular  aspiration  is  sufficient  effectivelj'^  to 
meet  the  altered  conditions,  and  prevent  extra  work  from 
being  thrown  upon  the  right  ventricle  when  compensation  is 
complete.  The  healtliiness  of  the  lungs,  and  the  freedom 
from  all  signs  of  pulmonary  congestion,  which  can  often  be 
seen  in  compensated  mitral  disease,  is  further  evidence  in 
support  of  this  view. 

MiD-DIASTOLIC    MiTKAL    MuRMUE 

This  theory  of  active  ventricular  expansion  also  suffices 
to  explain  the  mid-diastolic  murmur  of  mitral  stenosis,  much 
more  effectively  than  the  other  theory. 

The  loudness  of  this  murmur,  and  the  presence,  as  can 
often  be  noted,  of  a  well-marked  thrill  with  it,  points  to  its 
being  due  to  some  such  force  as  that  of  ventricular  aspiration, 
as  w^as  first  pointed  out  by  Ur.  Lockhart  Gibson,  then  of 
Edinburgh,  in  the  Lancet  for  1884  ;  as  was  also  the  fact  that 
this  murmur  often  increases  in  loudness,  as  compensation 
becomes  more  effective. 

The  muscular  nature  of  this  expansion  mo^'ement  also 
affords  an  explanation  of  the  reason  why  this  nuiimur  does 
not  occur,  as  it  might  reasonably  be  expected  to  do,  at  the 
time  of  the  closure  of  the  semilunar  valves,  when  the  blood 
is,  presumably,  beginning  to  enter  the  ventricle. 

This  explanation  will  probably  be  found  to  be  somewhat 
as  follows  : — 

During  the  expansion  phase,  the  cardiac  muscles,  as  already 
stated,  are  still  in  a  state  of  activity,  albeit  elongating  instead 
of  contracting,  and  the  muscuh  papillares  may  reasonably  be 
expected  to  partake  in  that  activity.  This  being  so,  it  is 
quite  possible  that,  during  the  whole  of  this  expansion  phase 
of  the  cardiac  cycle,  the  chordae  tendineae  are  kept  tense  by 
them,    and   although   the   aspirated   blood   is   flowing   freely 


394  EXPANSION  PHASE  OF  CARDIAC  CYCLE 

through  the  valve,  its  segments  (being  tense)  are  not  free  to 
vibrate  in  the  blood  stream. 

When,  however,  relaxation  comes  on  suddenly  at  the  end 
of  this  phase,  they  are  free  to  vibrate  in  the  blood  stream 
which  continues  to  flow  through  the  valve  under  the  momentum 
imparted  to  it  during  the  brief  expansion  phase. 

According  to  this  theory,  the  fixation  of  the  valve  segments, 
by  the  activity  of  the  musculi  papillares,  prevents  the  first 
inrush  of  the  blood  from  causing  an  early  diastolic  mm'mur 
in  mitral  stenosis,  and  delays  its  commencement  till  the 
onset  of  relaxation,  which  takes  place,  as  before  said, 
one-tenth  of  a  second  after  the  closure  of  the  semilunar 
valves.  To  this  delay,  the  murmur  owes  its  name  of  mid- 
diastolic (or,  as  it  used  to  be  called,  post-diastolic)  mitral 
murmur. 

If  the  second  sound  and  the  commencement  of  the  mid- 
diastolic murmur  are  recorded  by  an  electric  signal  upon  a 
revolving  drum,  it  will  be  found  that  the  interval  between 
them  is  about  a  tenth  of  a  second  ;  or,  if  the  murmur  is  recorded 
on  the  cardiogram,  it  will  be  found  to  occm'  at  the  point  where 
the  heart  muscle  relaxes. 

MiD-DiASTOLic  Murmur  in  Aortic  Eegurgitation 

Further  confirmation  of  this  theory,  as  to  the  mode  of 
production  of  the  mid-diastolic  murmur,  is  furnished  by  a 
murmm'  which  may  not  at  all  infrequently  be  heard  in  aortic 
regurgitation.  I  refer  to  a  so-called  presystoUc,  which  may  be 
mistaken  for  a  true  Austin  Flint  murmur. 

If  this  murmur  is  carefully  timed,  it  will  be  found  that  it 
follows  the  second  sound  by  the  same  interval  as  does  the 
mitral  mid-diastolic — namely,  a  tenth  of  a  second  ;  but,  as  in 
aortic  regm-gitation  the  heart  is  often  rapid,  and  the  diastole 
short,  this  interval  of  a  tenth  of  a  second  brings  it  so  near 
to  the  following  first  sound  of  the  heart  that  it  appears  to 
be  presystohc.  Nevertheless,  careful  timing  will  show  that 
its  relationships  are  with  the  second  sound  and  not  with  the 
first,  for  its  relationship  to  the  first  sound  alters,  when  the 
heart   alters  its  rate,  whereas  its  relationship   to  the  second 


EXPANSION  PHASE  OF  CARDIAC  CYCLE  395 

sound  remains  constant.  It  is,  therefore,  mid-diastolic  and 
not  presystolic. 

In  order  to  understand  this  murmur,  it  must  be  remembered 
that  the  anterior  cusp  of  the  mitral  valve  forms  the  posterior 
wall  of  the  channel  down  which  the  regurgitant  blood  flows 
in  aortic  regurgitation. 

During  the  expansion  phase,  while  the  valve  segments 
are,  according  to  supposition,  held  tense,  they  do  not  vibrate  ; 
but  if  the  regurgitation  is  sufficiently  prolonged  and  copious, 
it  will  cause  vibration  of  the  anterior  segment  of  the  mitral 
valve  at  the  onset  of  relaxation.  Careful  mapping  out  of  the 
area,  over  which  this  murmur  is  best  heard,  helps  to  confirm 
this  theory ;  for  it  is  often  best  heard  over  the  body  of  the 
right  ventricle,  internal  to  the  apex,  over  an  area,  where  the 
vibrations  of  the  anterior  cusp  of  the  mitral  valve  might  well 
be  conducted  to  the  anterior  wall  of  the  chest,  by  the  blood 
stream,  which  separates  it  from  the  muscular  tissue  of  the 
septum,  and  of  the  right  ventricle.  The  ordinary  mid-diastolic 
murmur  of  mitral  stenosis  is  not,  as  a  rule,  heard  over  this 
area  so  clearly  as  is  the.  Austin  Flint  murmur,  because  the 
channel  to  the  aorta  is  not,  in  this  case,  distended  with  blood, 
and  there  are  not,  therefore,  the  same  facilities  for  conduction 
to  the  anterior  wall  of  the  chest. 

In  some  cases,  the  mid-diastolic  aortic  regurgitant  murmur 
has  only  the  same  area  of  audition  as  the  mitral  mid-diastolic 
— namely,  at  and  internal  to  the  heart's  apex. 

This  explanation  is  further  upheld  by  the  observation  that 
sometimes  this  spm'ious  Austin  Flint  murmm-  is  quite  faint,  and 
is  simply  a  mid-diastolic  accentuation  of  the  ordinary  regurgi- 
tant murmur  audible  at  the  sternal  end  of  the  fourth  or  fifth 
left  interspace,  thus  showing  that  it  is  not  a  separate  murmur, 
produced  elsewhere,  but  is  due  to  the  vibration  of  the  same 
stream  of  blood,  which  is  producing  the  aortic  diastolic  murmm'. 

The  Third  Sound   of  the  Heart  ^ 

In  cases  in  which  the  flow  of  the  blood  is  not  strong  enough 
to  make  the  valve  segments  actually  vibrate,  the  onset  of 

'  See  Essa}'  XII. 


396  EXPANSION  PHASE  OF  CARDIAC  CYCLE 

relaxation  is  in  mitral  stenosis  marked  by  a  short  sound, 
which  is  heard  at  the  apex,  and  may  be  nearly  as  loud  as 
the  second  sound  itself,  but  follows  it  at  the  same  interval 
(a  tenth  of  a  second)  as  the  murmur  would  do. 

This  sound,  which  is  usually  called  a  '  spmious,'  or  'apical ' 
reduplication  of  the  second  sound,  is  well  known  as  occurring 
in  those  cases  of  stenosis  which  show  a  true  presystolic  murmur. 

This  third  sound  marks  the  commencement  of  the  third, 
or  relaxation,  phase  of  the  cardiac  cycle,  just  as  the  second 
sound  marks  that  of  the  second,  or  expansion,  phase. 

It  may  now  be  asked  why  this  third  sound  does  not  occur 
in  the  normal  heart  if  this  theory  is  correct,  and  the  answer 
is,  that,  in  the  normal  heart,  the  rapid  flow  of  blood  through 
the  mitral  valve  has  ceased  by  the  time  relaxation  sets  in, 
and  such  blood  as  may  then  be  passing  through  it  is  unable 
to  move  the  valves  suddenly  enough  to  produce  a  sound. 
The  reason  for  this  becomes  apparent,  if  the  size  of  the  mitral 
orifice  is  contrasted  with  the  capacity  of  the  amicle.  In  the 
normal  heart,  the  opening  is  wide  enough  to  allow  the  whole 
of  the  3-ounce  charge  to  pass  into  the  ventricle  dming  the 
expansion  phase,  in  spite  of  its  only  lasting  so  short  a  time ; 
for  the  diameter  of  the  full  auricle  would  be  about  2"  15  inches, 
and  the  diameter  of  the  mitral  orifice  is  1'18  inches. 

According  to  this  supposition,  anything  which  delays  the 
emptying  of  the  auricle,  and  so  leads  to  the  prolongation  of 
the  main  flow  of  blood  from  it  till  the  relaxation  sets  in,  ought 
to  produce  this  third  sound  of  which  we  are  speaking,  whether 
it  is  narrowing  of  the  mitral  orifice,  as  in  mitral  stenosis,  or 
an  excessive  amount  of  blood  in  the  auricle,  or  a  defective 
aspiratory  power  on  the  part  of  the  ventricle. 

The  correctness  of  this  theory  is  indicated  by  the  fact  that 
we  find  this  third  sound,  clinically,  in  just  such  cases  as  we  have 
indicated. 

We  not  infrequently  find  a  third  sound  present  over  the 
right  ventricle  in  anaemia,  due  to  either  or  to  both  of  the  last 
two  causes  we  have  just  enumerated,  for  the  ventricle  is  often 
acting  weakly  in  such  cases,  and  the  auricle  is  over-distended 
with  blood. 

A  third  sound  may  also  possibly  be  produced  in  the  manner 


EXPANSION  PHASE  OF  CARDIAC  CYCLE  397 

referred  to  earlier — namely,  by  the  mitral  valve  being  closed 
immediately  after  the  expansion  phase,  by  the  endeavour 
of  the  aspirated  blood  to  return  from  the  ventricle  back  into 
the  auricle  {vide  p.  388). 

This  early  closing  of  the  mitral  valve  may  be  the  cause 
of  the  third  sound  of  the  heart  in  some  cases  of  mitral  disease, 
and  it  is  also  possible  that  it  may  explain  the  occurrence 
of  a  third  sound  over  the  right  ventricle  in  certain  cases  of 
anaemia  with  dilatation  of  the  right  auricle. 

Compensatory  Dilatation  of  the  Left  Ventricle 

There  is  one  other  point,  where  this  theory  of  active  expan- 
sion solves  what  would  otherwise  be  a  problem  not  easy  of 
solution,  for  it  explains  the  compensatory  dilatation  of  the 
ventricle  in  mitral  regurgitation. 

It  is  evident,  where  the  mitral  valve  is  incompetent,  that  at 
the  end  of  the  systole,  the  auricle  must  contain,  in  addition 
to  its  normal  charge  of  3  ounces,  the  amount  which  has 
leaked  back  from*  the  ventricle.  This  additional  amount 
will,  therefore,  be  aspirated  into  the  ventricle,  during  its  ex- 
pansion phase,  and  will  cause  its  dilatation.  The  ventricle  is 
dilated  by  means  of  its  ovm  aspiratory  force.  Evidence  of 
this  is  given  by  cardiographic  records,  in  cases  of  mitral 
regurgitation,  for  a  sharp-pointed  rise  in  the  cardiogram  is 
often  observable  after  the  commencement  of  the  relaxation 
period,  due  to  the  impact  of  the  aspirated  blood  upon  the 
relaxed  ventricular  wall.^ 

It  is  not  always  very  safe  to  arrive  at  conclusions  by  a 
process  of  exclusion;  but,  in  the  present  instance, it  is  justifiable 
to  conclude  that  a  force,  which  can  distinctly  raise  the  lever  of 
a  cardiogi'aph  applied  over  the  left  ventricle,  after  the 
ventricular  wall  has  relaxed  (i.e.  aft^r  the  ventricular  and 
before  the  auricular  systole),  must  be  due  to  the  impact  against 
it  of  the  blood  which  has  been  set  in  motion  by  the  ventricular 
aspiration. 

The  mechanism  responsible  for  this  distension  of  the 
ventricle  during  its  relaxation  period  is  best  illustrated  by  a 

1  Essay  X.  p.  407,  and  Essay  XTI.  p.  433. 


398  EXPANSION  PHASE  OF  CARDIAC  CYCLE 

well-marked  case,  such  as  that  of  a  girl  who  died  in  the  General 
Hospital  from  mitral  regm-gitation,  and  with  adherent  peri- 
cardium. The  adhesion  having  been  prior  to  the  onset  of  the 
regurgitation,  the  rigidity  of  the  ventricular  wall,  thus  brought 
about,  prevented  compensatory  dilatation  of  the  left  ventricle 
from  taking  place.  The  result  was  that,  at  the  post-mortem, 
the  left  ventricle  was  practically  of  normal  size,  holding  only 
90  c.c,  whereas  the  left  auricle  held  164  c.c.  In  such  a  case  as 
this,  when  the  left  ventricle  expanded,  it  would,  by  its  suction, 
set  the  164  c.c.  in  motion,  and  the  momentum  of  the  blood 
would  tend  to  force  more  than  the  90  c.c.  into  the  ventricle. 
The  elasticity  of  the  ventricle,  strengthened  as  it  was  by  the 
adherent  pericardium,  would  expel  the  balance  over  and  above 
the  90  c.c.  back  into  the  auricle  through  the  leaky  mitral  valve. 
The  backward  reflux,  following  the  transient  over-distension, 
would  give  rise  to  just  such  a  sharp-pointed  wave  as  the 
cardiographic  tracing  showed. ^ 

The  case,  therefore,  shows  us  that  the  momentum  of  the 
blood,  aspirated  into  the  ventricle  during  its  expansion  phase, 
is  very  considerable,  and  is  able  to  over-distend  the  left 
ventricle  when  its  walls  are  relaxed. 

It  also  seems  reasonable  to  assume  that,  had  it  not  been 
for  the  pericardial  adhesions,  this  distensile  force  would  have 
been  amply  sufficient  to  cause  dilatation  of  the  ventricular 
cavity,  mitil  its  size  approximated  to  that  of  the  amicle  :  in 
other  words,  to  produce  the  necessary  com'pensatory  dilatation 
of  the  ventricle. 

In  this  case,  although  there  was  no  mitral  stenosis,  a  loud 
third  sound  was  audible  over  the  heart,  as  would  be  expected 
according  to  the  theory  of  its  causation,  as  already  stated. 

Where  the  right  ventricle  is  constricted  in  a  similar  way, 
by  adherent  pericardium,  a  similar  reflux  of  blood  from  the 
undilatable  ventricle  gives  rise  to  a  distinct  diastolic  impulse  in 
the  veins  of  the  neck,  and  the  presence  of  this  wave,  which  is 
clearly  visible,  is  a  sign  of  ill-omen  for  the  patient. 

These,  then,  are  the  points  in  favour  of  the  theory  of  cardiac 
action  which  I  am  advocating,  and  they  appear  to  me,  when 
taken  together,  to  give  undoubted  support  to  the  view  that 

'  Essay  X,  p.  407,  and  Essay  XII,  p.  433. 


EXPANSION  PHASE  OF  CARDIAC  CYCLE  399 

true  muscular  expansion  plays  a  most  important  part  in  the 
heart's  action. 

If  this  is  so,  it  would  be  well  to  alter  the  nomenclature  of 
some  of  the  heart's  sounds  and  murmurs  as  follows  : — 

The  first  sound  marks  the  commencement  of  ventricular 
contraction  or  systole. 

(Contraction  or  systolic  murmurs  may  be  produced  at 
mitral,  aortic,  tricuspid  valves,  &c.) 

The  second  sound  marks  the  commencement  of  expansion. 

(An  expansion  murmur  occurs  in  aortic  regurgitation.) 

The  third  sound  (when  present)  marks  the  onset  of  re- 
laxation. 

A  relaxation  murmur  may  occur  : — 

1.  In  mitral  stenosis,  &c. 

2.  Occasionally,  at  the  tricuspid  orifice  in  dilatation  of  the 

right  heart. 

3.  As  an  addition    to    the  expansion    murmur    in  aortic 

regurgitation,  j 


Essay  X.— THE  DIASTOLIC  EXPANSION  MOVEMENT 
OF  THE  VENTRICLES  AS  A  FACTOR  IN  COM- 
PENSATION FOR  DISEASE  OF  THE  ^MITRAL 
VALVE  1 

My  object  in  this  paper  is  to  bring  forward  evidence  in 
favour  of  the  heart  having  the  power  of  enlarging  its  chambers 
by  means  of  a  true  muscular  expansion  movement.  The 
possession  of  this  power  would  constitute  the  heart  a  double- 
acting  pump  instead  of  its  having  the  power  of  single  action 
only  with  which  accepted  theories  credit  it.  It  would  then  be 
able  to  fill  itself  by  its  own  counter  stroke,  just  as  is  the  case  with 
most  of  the  pumps  wdiich  the  art  of  man  has  devised.  The 
possession  of  such  a  powder  would  mean  that  the  heart  is  a  much 
more  perfect  mechanism  than  if  it  had  to  depend  upon  some 
extraneous  mechanism  for  the  tilUng  of  its  ventricles,  as  the 
ordinarily  accepted  theory  asserts. 

This  view — ^that  the  ventricles  of  the  heart  possess  the 
power  of  aspiration  in  virtue  of  a  true  vital  expansion  of  its 
muscular  fibres — ^was,  I  beheve,  first  definitely  propounded  by 
Dr.  Lockhart  Gibson,  when  assistant  to  the  late  Professor 
Rutherford,  some  sixteen  years  ago.^  He  pointed  out  that 
in  the  case  of  ordinary  striated  muscular  fibre  the  phase  of 
contraction,  which  results  from  a  minimal  stimulation  of  the 
muscle,  is  followed  by  a  phase  of  sudden  expansion,  during 
which  the  muscle  develops  about  two-fifths  of  the  force  it 
develops  during  contraction,  but  in,  of  course,  the  reverse 
direction.  The  possession  of  such  an  expansile  power  by  the 
individual  muscular  fibres  of  the  heart  would  cause  a  sudden 
and  moderately  powerful  enlargement  of  the  ventricles  at  the 
commencement  of  the  disastole. 

^  In  part  taken  from  a  thesis  (Gold  Medal)  for  the  degree  of  M.D.  at 
the  University  of  Edinburgh,  1892.  Vide  the  British  Medical  Journal,  Sep- 
tember 29,  1900. 

2  Lancet,  April  19,  1884,  p.  730. 

400 


VENTRICULAR  EXPANSION  401 

Physiological  Evidence  as  to   the  Nature  of  the 
Expansion  Movement  of  the  Ventricles 

So  far  as  I  have  been  able  to  ascertain,  there  is  but  little 
experimental  evidence  that  the  expansion  of  the  ventricles 
is  due  to  a  muscular  movement  in  addition  to  simple  elastic 
resihency.  We  know,  however,  that  the  muscular  fibre  of  the 
ventricles  remains  active  for  an  appreciable  time  after  the 
closure  of  the  semilunar  valves,  and  does  not  at  once  enter 
upon  its  phase  of  relaxation.  The  most  striking  physiological 
evidence  of  the  possession  of  such  a  power  which  I  have 
been  able  to  find  is  afforded  by  some  experiments  made  by 
Stephani  and  quoted  by  Tigerstedt.^  He  found  that  section 
of  the  vagus  nerve  diminished  the  force  of  the  heart's  recoil 
after  contraction.  When  the  vagus  was  divided,  less  force 
was  required  to  prevent  the  diastohc  enlargement  of  the  heart 
than  was  necessary  before  section  of  the  vagus. 

The  confirmation  of  this  observation  would  seem  to  prove 
•that  the  expansion  of  the  heart  is,  in  part  at  all  events,  a 
muscular  movement  under  nervous  control,  and  not  simply 
a  mechanical  phenomenon  due  to  elasticity  only. 

Clinical  Evidence    of   the   Nature    of   the   Expansion 
Movement  in   the  Normal  Heart 

Clinically,  we  have  httle  opportunity  of  studying  the  changes 
in  volume  which  the  heart  undergoes  during  its  phases  of 
contraction  and  expansion.  Were  instantaneous  radiography 
of  the  heart  possible,  we  should  have  an  excellent  means. 

Om'  chief  som'ce  of  information  is  the  cardiograph.  There 
are  difficulties  and  fallacies  connected  %vith  the  use  of  the 
cardiograph  of  which  we  must  take  account.  Of  these  the 
interpretation  of  the  cardiogram  is  perhaps  the  most  important. 
This  I  have  in  large  measm-e  overcome  by  the  simultaneous 
record  of  the  cardiac  sounds  upon  the  cardiogram.  This  can 
be  done  by  means  of  an  electric  time-marker,  which  makes 
an  audible  chck  as  it  rises  and  falls.  It  is  quite  easy  in  most 
cases  to  synchronise  the  chcks  of  the  electric  signal  with  the 

^  Phys.  des  Kreislaufes,  p.  143. 

2  D 


402  EVIDENCE  AS  TO 

heart  sounds,  and  thus  to  distinguish  between  the  systohc 
and  the  diastohc  portion  of  the  cardiogram. 

In  the  course  of  the  last  nine  years,  since  I  first  used  this 
method,  I  have  had  ample  evidence  of  its  reliabihty  ;  and, 
further,  I  think  I  can  claim  that  the  beautiful  researches 
of  M.  A.  Chauveau,  upon  the  movement  of  the  cardiac  valves 
in  relation  to  the  intracardial  pressure  curves  and  the  cardio- 
gram,^ fully  confirm  the  interpretation  of  the  cardiograms 
which  I  am  about  to  give. 

In  using  the  cardiograph  for  the  study  of  the  expansion 
movement  of  the  heart,  we  must  remember  the  limited  area 
over  which  we  can  take  tracings,  and  give  due  allowance 
for  the  changes  in  form  which  may  occur  apart  from  alterations 
in  the  volume  of  the  heart. 

Evidence   obtained   prom    the  Study   of   the   Heart   in 
Valvular  Disease 

When  considering  the  process  of  compensation  for  incom- 
petence or  stenosis  of  the  mitral  valve,  the  possession  of  such 
a  muscular  power  as  we  are  discussing  would  be  of  very  great 
service  to  the  heart.  In  the  case  of  mitral  incompetence 
the  occurrence  of  hypertrophy  and  dilatation  would  increase 
the  aspiratory  power  equally  with  the  expulsive  power.  If 
this  were  so,  w^e  would  expect  in  a  case  of  compensated  mitral 
regurgitation  that  there  would  be  little,  if  any,  backward 
pressure  on  the  lungs  or  right  side  of  the  heart,  and  that  the 
left  auricle  would  have  no  more  than  a  normal  amount  of  work 
to  do. 

Pathological  Evidence 

In  the  only  cases  of  mitral  regurgitation  with  unbroken 
compensation  which  I  have  been  able  to  examine  post-mortem 
there  was  evidently  much  regurgitation,  and  the  left  ventricle 
was  much  dilated,  but  the  left  auricle  was  of  almost  normal 
size,  suggesting  that  the  hypertrophy  and  dilatation  called 
forth  by  the  failure  in  expelhng  power  was  fully  sufficient 
for  compensation  so  far  as  aspiration  also  was  concerned. 

1  Jour,  de  lyhysiol.  2Mlhol  1899-1900. 


VENTRICULAR  EXPANSION  403 

In  the  first  of  the  cases  the  left  ventricle  held  165  c.c.  as 
against  the  normal  80  c.c,  while  the  left  auricle  held  the 
normal  90  c.c.  In  the  other  case  the  left  ventricle  held 
235  c.c.  as  against  the  normal  80  c.c. ;  the  left  amicle 
only  held  115  c.c.  Considering  that  it  is  quite  usual  for  the 
left  auricle  to  be  dilated  to  the  extent  of  120  c.c.  in  patients 
dying  of  pneumonia  and  other  diseases  without  definite  cardiac 
disease,  these  figures  are  remarkable,  and  cannot,  so  far  as  I 
can  see,  be  explained  by  the  ordinarily  accepted  theory  of 
compensation  in  mitral  regm-gitation.  They  are,  I  consider, 
strong  evidence  in  favour  of  what  I  may  call  the  '  vis  a  f route  ' 
theory  of  compensation — namely,  that  the  ventricle  by  increase 
in  its  aspiratory  power  compensates  for  the  incompetence  of 
the  mitral  valve,  and  that  so  long  as  compensation  remains 
unbroken  the  left  auricle  and  right  side  of  the  heart  have  very 
httle  extra  strain  put  upon  them. 

In  comparison  with  the  above  figures  those  of  another 
case  (Case  IV)  are  striking.  Here  compensation  had  failed, 
and  while  the  left  ventricle  only  held  200  c.c,  as  compared 
with  the  235  c.c.  above  mentioned,  the  left  amicle  held  250  c.c 
as  against  the  115  cc.  where  compensation  was  good.  In  such 
a  case  there  was  undoubtedly  extra  strain  on  the  left  auricle 
and  right  ventricle. 

Cardiographic  Evidence  in  Mitral  Regurgitation 

In  mitral  regurgitation,  we  have  cardiograph] c  evidence 
of  increased  diastolic  expansion  of  the  ventricles.  I  show 
some  tracings  taken  from  cases  of  mitral  incompetence,  and 
side  by  side  with  them  some  from  normal  hearts.  The  time 
of  occurrence  of  the  heart  sounds  is  marked  on  some  of  them. 
In  tracings  taken  over  the  apex  beat,  the  tilt  of  the  heart's 
apex  hides  any  movement  due  to  change  in  volume,  because, 
as  has  long  been  known,  the  apex  remains  pressed  against  the 
chest  wall  for  an  appreciable  time  after  the  closm'e  of  the 
semilunar  valves.  In  tracings  taken  over  the  ventricle  internal 
to  the  apex,  the  diminution  in  the  size  of  the  ventricle  during 
systole  causes  the  heart  to  recede  from  the  chest  wall,  and  we 
have  more  or  less  of  a  systolic  depression  in  the  cardiogram 

2  D  2 


404  EVIDENCE  AS  TO 

{vide  Plate  VII,  Case  I,  figs.  3  aud  4).  In  such  a  situation  the 
enlargement  of  the  heart,  after  the  systole,  may  also  be  expected 
to  show  as  a  rise  in  the  cardiogram  if  sufficiently  powerful. 
In  taking  my  tracings,  I  used  a  pressure  of  about  I  lb.  in  the 
spring  of  my  cardiograph,  and  therefore  any  elevation  seen  in 
the  tracings  I  show  imphes  that  the  heart  wall  was  able  to 
overcome  a  resistance  of  at  least  |  lb.  in  causing  the  elevation 
of  the  lever. 

I  show  some  tracings  from  a  normal  heart  where  there  is 
some  evidence  of  sudden  enlargement  at  the  time  of  the  closure 
of  the  semilunar  valves  (Plate  VII,  Normal  Heart,  fig.  2). 

I  also  show  some  tracings  taken  over  the  right  ventricle 
in  a  case  of  anaemic  dilatation.  They  show  very  well  the 
sudden  enlargement  of  the  ventricle  after  the  systole  (Plate  VII, 
Case  I,  tigs.  2,  3,  and  4).  The  fact  of  the  lever  of  the  cardio- 
graph rising  so  rapidly  and  powerfully  is  proof  that  the  ventri- 
cular wall  does  not  relax  till  after  a  certain  amount  of  expansion 
has  occurred,  otherwise  it  would  not  have  strength  to  hft 
the  lever.  I  may  say  that  this  is  quite  an  ordinary  type 
of  tracing.  In  comparison  with  these,  I  show  some  tracings 
from  a  case  of  moderate  mitral  regurgitation.  In  this  series 
the  diastolic  expansion  "wave  is  well  marked  (Case  II). 

In  the  next  two  series  (Cases  III  and  IV)  there  was  very 
considerable  regm-gitation.  In  the  first  the  systolic  diminution 
in  size  of  the  ventricle  is  much  more  rapid  than  normal, 
as  might  be  expected,  and  the  diastoHc  expansion  rise  is 
proportionately  more  marked.  In  the  next  (Case  IV),  there 
was  very  extreme  mitral  regurgitation,  the  cavity  of  the  left 
ventricle  was  enlarged  to  more  than  twice  its  natural  size, 
its  contents  being  7  omices  (200  c.c.)  instead  of  the  normal 
2^  ounces  (80  c.c.) ;  the  contents  of  the  left  auricle  were 
9  ounces  (250  c.c).  In  this  case  the  systohc  diminution 
was  so  extreme  and  the  diastohc  expansion  so  great  that  the 
tracing  is  divided  into  two  nearly  equal  halves  by  a  deep 
notch. 

Case  V. — Finally,  I  show  you  some  tracings  taken  over 
the  right  ventricle  in  a  case  of  mitral  regm-gitation  with  ex- 
treme secondary  tricuspid  regui'gitation.  So  extreme,  indeed, 
was  the  regm-gitation  that  a  systohc  thriU  could  be  felt  over 


VENTRICULAR  EXPANSION  405 

the  right  auricle  in  the  region  of  the  right  nipple.  The 
tracings  are  extremely  interesting  but  too  complicated  to  be 
fully  explained  within  the  limits  of  this  essay.  I  show  you, 
however,  a  series  from  the  outer  part  of  the  fifth  left  interspace. 

I  have  proved  the  correctness  of  the  interpretations  given 
in  the  figures  by  means  of  many  observations  with  the  electric 
recorder  of  the  heart  sounds,  and  by  the  polygi'aph,  and  also 
by  taking  consecutive  series  of  tracings  |-inch  apart  over  the 
available  part  of  the  heart.  The  diastolic  expansion  wave 
is  here  very  high,  and  in  tracings  taken  in  the  fifth  interspace 
in  the  nipple  Hne — ^the  apex  being  in  the  axilla — this  part  of  the 
tracing  is  far  higher  than  the  rest  (vide  Plate  XII). 

In  fig.  5  is  shown  a  polygraph  tracing  taken  with  a  Marey's 
drum  cardiograph,  with  the  heart  sounds  recorded  on  it.  It 
shows  that  the  closure  of  the  semilunar  valves  occm-s  at  the 
notch  about  half-way  up  the  diastoHc  expansion  rise.  It  is 
difficult  for  me  to  believe  that  these  phenomena  can  be  explained 
on  the  supposition  of  the  expansion  movement  being  simply 
a  mechanical  one  due  to  the  elastic  recoil  of  the  relaxing  heart 
wall.  There  is  far  more  and  far  stronger  movement  than  could 
be  explained  except  by  a  true  muscular  expansion  movement. 

Clinical  Evidence  in  Mitral  Stenosis 

In  mitral  stenosis,  we  have  clinically  various  phenomena 
more  or  less  indicative  of  increased  diastolic  activity  on  the 
part  of  the  ventricles.  In  the  first  place,  there  is  sometimes 
post-mortem  evidence  that  the  left  ventricle  has  increased  work 
to  do.  Its  wall  sometimes  seems  to  be  shghtly  thicker  than 
normal.  Secondly,  the  first  sound  of  the  heart  is  louder  than 
normal  in  mitral  stenosis.  Now  the  ventricle  has,  if  anything, 
a  diminished  amount  of  work  to  do  so  far  as  its  direct  or  forward 
work  is  concerned,  owing  to  the  hindrance  to  the  fiUing  of  the 
ventricle,  and  we  ought  therefore  to  expect  that  the  first  sound 
would  not  be  louder  than  normal.  Thirdly,  the  first  sound 
ends  more  sharply  than  normal. 

The  explanation  of  these  facts  is,  I  believe,  that  the  ventricle 
alters  its  beat.  It  contracts  with  greater  force  and  suddenness, 
in  order  that  the  recoil — both  elastic  and  muscular — may  be 


406  EVIDENCE  AS  TO 

as  great  as  possible,  thus  developing  the  maximum  amount  of 
aspiration.  In  this  way  the  ventricle  by  its  altered  beat  is 
able  to  compensate  for  the  valvular  disabiUty,  without  there 
being  any  permanent  need  for  increased  action  of  the  right 
heart.  Every  practitioner  must  know  many  cases  of  mitral 
stenosis  which  are  fully  compensated,  and  where  there  is  no 
evidence  at  all  of  any  increased  blood  pressure  in  the  lungs. 
According  to  the  ordinary  accepted  vis  a  tergo  theory  of  com- 
pensation, there  must  be  increased  pulmonary  blood  pressure 
in  all  cases  of  stenosis.  According  to  the  vis  a  fronte  theory, 
this  is  not  necessary,  and  the  clinical  facts  seem  to  me  more 
in  favour  of  the  latter  than  the  former. 

I  shall  deal  with  the  other  chnical  evidence  of  increased 
aspirator}^  action  after  dealing  with  the  cardiographic  evidence. 

Cardiographic  Evidence   in  Mitral  Stenosis 

Owing  to  the  ventricle  filling  more  slowly  than  normal, 
we  expect  the  expansion  wave  to  be  less  marked  than  normal, 
and  we  shall  not  expect  it  to  show  in  the  cardiogi-aphic  tracings. 
This  is  so  {vide  Case  YI,  figs.  1,  2,  and  3).  Although  the 
expansion  movement  itself  does  not  show  in  the  tracing,  we 
very  often  have  an  accessory  wave  which  gives  us  very 
important  evidence  as  to  the  presence  of  a  powerful  aspiratory 
action.  I  refer  to  a  small  sharp  wave  which  occurs  just  after 
the  diastolic  expansion  movement  has  ceased — namely,  imme- 
diately after  relaxation  of  the  cardiac  muscle  has  occurred. 
This  wave  is  best  seen  at  and  near  the  apex  {vide  Cases  YII 
and  VIII),  but  is  sometimes  evident  over  a  considerable  part  of 
the  heart.  The  cause  of  this  wave  is,  I  beheve,  as  follows  :  At 
the  commencement  of  diastole  the  left  auricle  is  naturally  con- 
siderably distended  with  blood,  and  the  ventricular  aspu-ation 
causes  it  to  rush  into  the  ventricle  with  considerable  force. 
Owing  to  the  narrowness  of  the  mitral  orifice  it  enters  more 
slowly  than  normal,  and  there  is  not  time  for  all  the  blood  to 
get  through  into  the  ventricle  before  the  expansion  movement 
ceases.  "SAlien,  therefore,  relaxation  commences  there  is 
still  a  strong  stream  of  blood  flowing  into  the  ventricle.  It  is 
the  impact  of  this  stream  upon  the  relaxed  heart  wall  that 


VENTRICULAR   EXPANSION  407 

causes  the  small  rise  referred  to.  (This  wave  is  clearly  not 
due  to  the  auricle,  because  when  the  heart  is  irregular  this 
wave  maintains  a  constant  relation  to  the  beat  which  precedes 
it,  while  its  distance  from  the  following  beat  is  variable 
{vide  fig.  142,  p.  432). 

Suction  Eecoil  Wave 

If  this  theory  be  correct,  we  ought  to  see  this  wave  (which 
I  call  the  suction  recoil  wave)  whenever  the  auricle  is  not  able 
to  discharge  the  bulk  of  its  contents  into  the  ventricle  before 
the  onset  of  relaxation.  I  show  a  tracing  (Case  VII)  from  a 
case  where  there  was  considerable  mitral  regurgitation  with  no 
stenosis,  but  where  the  ventricle  could  not  dilate  to  its  proper 
amount  in  consequence  of  pericardial  adhesions.  The  cubic 
content  of  the  left  ventricle  was  90  c.c,  and  that  of  the 
left  auricle  164  c.c.  In  this  case  the  suction  recoil  wave 
was  most  marked  {vide  p.  433). 

This  suction  recoil  wave  is  closely  associated  with  a  diastoHc 
cardiac  sound  which  is,  I  believe,  due,  like  it,  to  the  aspiratory 
power  of  the  ventricle.  I  refer  to  the  so-called  reduplicated 
second  sound  which  is  heard  at  the  apex  in  mitral  stenosis. 
This  sound  has  no  right  to  be  called  a  second  sound.  It  can 
easily  be  demonstrated  that  it  is  neither  the  aortic  nor  the 
pulmonary  second  sound.  With  a  differential  stethoscope  it  is 
frequently  easy  to  hear  all  three  sounds.  This  sound  ought 
to  have  a  name  of  its  own,  and  I  have  named  it  the  '  third 
sound '  of  the  heart,  and  called  it  so  for  many  years.  It  has 
been  described  by  some  authors  as  the  sound  of  the  mitral 
opening.  This  is,  I  believe,  not  quite  correct,  for  it  is  produced 
shortly  after  the  opening  of  the  mitral  valve.  I  have  in  many 
instances  recorded  the  time  of  occurrence  of  this  sound  on  the 
cardiogram,  and  I  find  that  it  usually  coincides  exactly  with  the 
commencement  of  the  suction  recoil  wave  just  spoken  of.  I 
beheve  that  this  sound  is  caused  by  the  im'ush  of  blood  into 
the  ventricle  at  the  commencement  of  diastole,  as  was  suggested 
by  Dr.  Sansom,  twenty  years  ago,^  but  the  exact  mechanism 
of  its  production  I  believe  to  be  as  follows  : — 

Dm'ing   the   phase   of   diastolic   expansion,  the  auriculo- 

^  Proc.  of  Med.  Soc.  of  London,  vol.  v.  p.  199  et  seq. 


408  EVIDENCE  AS  TO 

ventricular  valve  is  kept  more  or  less  rigid  by  the  tension  of 
the  chordae  tendinesD.  As  soon,  however,  as  relaxation  sets 
in,  the  valve  is  free  to  move,  and  if  the  auricle  has  not  already- 
been  emptied  by  the  aspiration  during  the  expansion  movement, 
the  in-rushing  blood  stream  will  flap  the  valve  back  against 
the  ventricle  wall  in  a  manner  calculated  to  produce  the  faint 
sound  we  are  speaking  of. 

Mitral  Mid-diastolic  Murmur 

I  now  come  to  the  last  of  the  physical  signs  in  mitral  stenosis 
of  which  I  wish  to  speak — namely,  the  mitral  diastolic  murmur. 
By  this  murmur,  I  mean  the  one  sometimes  called  post- 
diastolic, because  of  its  occurring  after  the  second  sound, 
not  with  it  as  in  the  case  of  the  aortic  diastolic  murmur. 
This  murmur  is  also  sometimes,  I  believe,  called  a  mid- 
diastolic murmur.  It  begins  loudly  and  then  fades  away, 
although  sometimes  prolonged  through  the  diastole.  Its 
time  relation  to  the  second  sound  is  constant,  but  its 
relation  to  the  first  is  not  constant,  the  reverse  being  true 
of  the  presystolic.  This  murmur  is  now,  I  beheve,  very 
generally  recognised  as  being  a  suction  murmur  and  due  to 
ventricular  aspiration,  and  the  fact  that  it  is  very  often 
strong  enough  to  give  rise  to  a  palpable  thrill  is  evidence 
as  to  the  force  of  the  aspiration. 

On  studying  the  relation  of  this  murmur  to  the  '  third 
sound  '  of  the  heart  it  is  evident  that  the  two  are  closely  related. 
The  murmur  occurs  at  the  same  interval  of  time,  after  the 
second  sound,  that  the  third  sound  does  ;  and  in  cases  where  the 
third  sound  is  audible,  a  slight  alteration  in  the  rate  or  strength 
of  the  heart  will  frequently  transform  the  third  sound  into  the 
mid-diastohc  murmur  and  vice  versa.  The  mid-diastolic  murmur 
may  accompany  or  replace  the  third  sound.  Also  on  recording 
the  time  of  this  murmur  on  the  cardiogram  it  is  found  to 
coincide  with  the  suction  recoil  wave  just  as  the  third  sound 
does.  The  explanation  given  for  the  third  cardiac  sound 
holds  true,  I  think,  for  this  murmur.  The  valve  segments  are 
not  free  to  vibrate  in  the  blood  stream  till  after  the  muscular 
relaxation  has  set  in. 


VENTRICULAR  EXPANSION  409 


Cardiogram  in  Aortic  Regurgitation 

The  last  point  to  which  I  wish  to  draw  attention  in  this 
essay  is  the  evidence  given  by  the  cardiogram  in  aortic  regurgi- 
tation. If  the  diastolic  expansion  movement  were  pm-ely  a 
mechanical  one  it  ought  to  be  evident  in  aortic  regurgitation 
as  it  is  in  mitral  regurgitation.  The  cardiogram  shows  that 
this  is  not  so.  A  marked  feature  of  all  the  tracings  I  have  taken 
in  aortic  regurgitation  is  the  absence  of  the  diastohc  expansion 
wave.  The  tracings  shown  under  Case  IX,  fig.  1,  and  Case  X 
illustrate  this  point,  and  show  the  absence  of  the  expansion 
wave. 

In  giving  these  tracings  as  typical  of  the  cardiogram  in 
aortic  regurgitation,  I  ought  to  add  that  my  generalisation  as  to 
aortic  disease  is  only  based  upon  the  cardiographic  study  of  some 
eight  or  ten  cases.  There  was,  however,  sufficient  similarity 
in  the  tracings  obtained  to  make  it  admissible  to  generalise 
from  so  few  a  number.  The  reason  for  this  type  of  tracing 
is  evident,  for  in  aortic  regurgitation  increase  of  ventricular 
aspiration  would  only  increase  the  amount  of  leakage.  The 
heart,  therefore,  alters  its  beat  so  as  to  produce  a  minimal 
amount  of  diastohc  expansion. 

The  tracings  in  aortic  regurgitation,  therefore,  give  us 
most  important  evidence  that  the  expansion  movement  is  one 
under  nervous  control  and  not  a  simple  mechanical  one. 

In  bringing  this  essay  to  a  conclusion,  I  am  conscious 
that  much  of  it  is  theory,  and  therefore  may  be  erroneous. 
But  as  a  result  of  many  years'  careful  observation  and  research, 
I  have  been  unable  to  obtain  any  evidence  except  such  as  seems 
to  point  strongly  in  favour  of  the  expansion  of  the  ventricles 
being  in  large  measure  due  to  a  true  muscular  movement. 


410  EVIDENCE  AS  TO 


EXPLANATION  OF  PLATES  VII  AND  VIII 

The  tracings  are  all  to  be  read  from  left  to  right. 

They  were  all  taken  with  a  Calabin's  cardiograph,  except  Case  V  (fig.  5) 
and  CaF3e  VI  (fig.  .3).  These  two  wore  taken  with  a  Marey's  drum  cardiograph 
and  tambours. 

The  systolic  portion  of  the  cardiogram  is  enclosed  between  broken  lines, 
and  is  marked  by  a  black  band  at  the  foot  of  each  tracing.  The  position 
of  the  lino  marking  the  close  of  the  ventricular  systole  has  in  most  of  the 
instances  hero  given  been  ascertained  by  recording  on  the  cardiogram  the 
time  of  occurrence  of  the  second  sound.  In  the  remainder  it  has  been  inferred, 
owing  to  the  similarity  of  the  tracings  to  others  in  which  the  time  of  occurrence 
of  the  second  sound  had  been  recorded.  This  line  marks  the'  commencement 
of  the  period  of  rapid  diastolic  expansion  of  the  ventricles.  The  close  of  this 
expansion  period  (i.e.  the  commencement  of  complete  ventricular  relaxation) 
is  marked  by  a  dotted  line.  At  the  foot  of  each  figure  the  portion  of  the 
cycle  occupied  by  the  expansion  period  is  marked  by  a  dotted  band. 


Plate  VII 

Case  I. — Anaemia  with  Dilatation  of  the  Heart. — The  apex  was  in  the 
fourth  interspace,  3 J  inches  out  from  the  sternum.  Figs.  1,  2,  3,  and  4  are 
tracings  taken  in  the  fourth  interspace  at  distances  of  3^  inches,  3  inches, 
2|  inches,  and  2^  inches  respectively  from  the  sternum.  They  show  the  gradual 
substitution  of  a  systolic  depression  for  the  systolic  elevation  .shown  in  the 
apex  tracing.  This  depression  is  due  to  the  withdrawal  of  the  heart  from 
the  chest  wall,  owing  to  its  systolic  diminution  in  volume.  These  latter 
tracings  show  a  well-marked  expansion  rise  at  the  commencement  of  diastole. 

Case  II. — Mitral  Regurgitation  with  Anemia. — Fig.  1,  tracing  from  the 
apex  in  the  sixth  interspace,  3  inches  out  from  the  sternum  (i.e.  |  inch  external 
to  the  nipple  iine).  Figs.  2,  3,  4,  and  5  are  tracings  from  the  fifth  space,  at 
distances  from  the  sternum  of  3  inches,  2J  inches,  21  inches,  and  about  2^  inches 
respectively. 

They  show,  as  in  Case  I,  the  substitution  of  a  systolic  depression  for  the 
sy.stolic  elevation  of  the  apex  cardiogram,  and  they  show  a  well-marked  diastolic 
expansion  rise. 

Case  III. — Con.siderable  Mitral  Regurgitation. — The  apex  was  in  the 
sixth  space,  2  inches  external  to  the  nipple  line.  The  apex  cardiogram  was  similar 
to  Case  II,  and  is  not  given.  Fig.  1  and  fig.  2,  tracings  from  the  fifth  space, 
2  inches  and  1  inch  out  from  the  sternum.  Both  tracings  show  the  expan.sion 
movement  well,  but  especially  fig.  2. 

Normal  heart,  from  a  case  of  fibroid  phthisis,  with  retraction  of  the  left 
lung.  Fig.  1  and  fig.  2,  cardiograms  taken  at  the  apex  just  internal  to  it.  The 
latter  shows  a  slight  amount  of  diastolic  expansion. 


PLATE  VII 

Cardiograms  Demonstrating  the  Enlargement  of  the  Ventricle 
DURING  ITS  Expansion  Phase 


.        CASEI.      ^      ^^CASEH.     ^      ^CASEn. 

Anaemic  Mdtdtion.  Mitral  leprg:iCdtiorL.  GredCMiCmlEegiirgitation. 


1^1 

mm 

m 

or" 

yo 

O  X 

n> 

3-D 

e- 

CT?) 

a. 

CT 

CTO 

O  3 

o 

3 

(For  the  explanation  of  the  tracings,  see  oppoaite  page.) 


PLATE  VIII 

Cardiograms  Demonstratinc;  the  Enlar(!eme.\t  of  the  Ventricle 
DURING  ITS  Expansion   Phase 


CASE  IV. 


CASEv. 


CASEvr. 


"Verjg-redCMitol      ....       Very  ^reaC  MitoU  HidraJ.  SCenosis. 


TgiCdCion.  \    \  \   \    \\ 


Him 

■  mi           ■inn 

6';'' space  arouC. 

CASETI. 

Mitral  Stenosis. 


CASEv:  Tracing  showing  prominent; 
Expansion  Wdve 


Record  of  isC5(  and  heart  sound 


CASE  VII 

al  Reg-urg-iL^., 
with  3^  Sound 


,    ,,     CASEX. 

Aoruic  Reprg-itdtion 


Mi'^rdl.Re&urg^itdtion   \,\  \    *^^'  ^ 


Record  of  i^&£".<^ sound 5 


5"^^  space       st^Spa-ce,    \M\\   \ 
2'ouC  iijouC.^    •■■^ 


Showing'  record  of  i^.'',  2".''  h  i'i  sounds  on 
cardiogram. 

,    ,.  CASE  El. 

Aortic^  RegTirptaticn 

s'i^spdce^ 


^4  ouC.  }  \\\ 


,.,^,     CASE  vnr. 
With  veiy  loud  i"?-  Sound  & 
prominent  Suction  Recoil 
.  Wave         W 


^^^°^^^^^^^t^-^^^A 


(For  the  explanation  of  the  tradngs,  see  opposite  page.) 


VENTRICULAR  EXPANSION  411 


Plate  VIII 

Case  IV. — Very  extreme  Mitral  Regurgitation. — The  apex  beat  was  in 
the  sixth  space  in  the  anterior  axillary  line.  Fig.  1  from  the  sixth  space,  ^  incli 
internal  to  the  nipple  line.  Fig.  2  from  the  fifth  space,  IJ  inches  from  the 
sternum.     They  show  an  extremely  well-marked  diastolic  expansion  wave. 

Case  V. — Great  Mitral  and  Tricuspid  Regurgitation. — The  apex  was  in 
the  sixth  space  in  the  anterior  axillary  line,  4  inches  from  the  sternum.  Figs.  1, 
2,  and  3,  cardiograms  from  the  sixth  space  at  distances  of  3^,  2  J.  and  H  inches 
from  the  sternum.  Fig.  4  from  the  fifth  space,  IJ  inches  out.  Fig.  1  is  of 
the  apex  type.  The  remainder  show  an  extremely  pronounced  diastolic 
expansion  movement.  The  interpretation  here  given  was  verified  by  very 
numerous  observations  and  records  of  the  heart  sounds  on  the  cardiogram. 
Fig.  5  is  a  tracing  similar  to  No.  4,  but  taken  with  the  polygraph  and  with  a 
record  of  the  first  and  second  sounds  on  the  tracing. 

Case  VI. — Mitral  Stenosis,  with  a  well-harked  Third  Sound  and 
Mitral  diastolic  murmur. — The  diastolic  expansion  movement  does  not  show 
at  all,  but  there  is  a  well-marked  wave  at  the  commencement  of  the  relaxation 
period — a  suction  recoil  wave.  Fig.  1,  from  sixth  space,  4  inches  out  from 
sternum,  and  fig.  2,  3^  inches  from  sternum.  Fig.  3,  similar  tracing  to  1,  but 
taken  with  the  polygraph,  and  showing  the  position  of  the  first,  second,  and 
third  sounds,  as  recorded  on  the  cardiogram. 

Case  VII. — Mitral  Regurgitation,  with  a  well-marked  Third  Sound, 
BUT  NO  stenosis. — Tracing  taken  from  near  the  apex,with  a  record  of  the  first 
and  second  sounds  on  the  cardiogram.  The  sounds  in  this  case  Avere  also  re- 
corded separately,  and  careful  measurements  showed  that  the  third  sound  w  ould 
come  just  at  the  foot  of  the  sharp  rise  which  occurs  between  the  beats. 

Case  VIII.— Mitral  Disease,  with  well-makk;ed  Third  Sound. — The 
third  sound  was  louder  than  the  first  sound  and  as  loud  and  distinct  as  the 
second  sound.  The  time  of  the  first  and  second  sound  is  recorded  on  the 
cardiogram.    There  is  a  prominent  suction  recoil  wave  as  in  the  preceding  case. 

Case  IX. — Aortic  Regurgitation. — Tracing  from  the  fifth  space  ^  inch 
from  the  sternum,  showing  absence  of  the  diastolic  expansion  rise.  Below  this 
is  placed  for  comparison  a  cardiogram,  from  a  similar  part  of  the  heart,  from 
Case  III.,  with  mitral  regurgitation,  where  there  is  a  prominent  expansion  rise. 

Case  X. — Aortic  Reguritation. — Tracing  from  near  the  apex  showing 
smallness  of  the  expansion  wave.  Compare  Case  I,  figs.  1  and  2 ;  Case  II 
figs.  2  and  3  ;  and  Case  V,  figs.  1  and  2- 


Essay  XL— ON  THE  THEOEY  OF  COMPENSATION 
IN  INCOMPETENCE  AND  STENOSIS  OF  THE 
MITKAJj  VALVE  ^ 

The  object  of  this  essay  is  to  make  a  clinical  contribution 
towards  the  proof  of  what  may  be  called  the  modern  theory 
of  compensation  in  disease  of  the  mitral  valve. 

For  the  last  fifteen  or  sixteen  years  the  belief  has  been 
gaining  gi'omid  that  the  filling  of  the  left  ventricle  of  the  heart 
during  diastole  is  mainly  due  to  aspiration  by  the  ventricle 
itself  rather  than  to  the  contraction  of  auricle  or  other  forces. 

This  view  as  to  the  filling  of  the  ventricle,  w^hich  is  based 
upon  observations  such  as  those  of  Dr.  H.  D.  EoUeston  (who 
demonstrated  the  presence  of  a  negative  pressure  in  the  ventricle 
during  diastole),  has,  since  1885  or  earlier,  been  advocated 
by  some  writers  and  lecturers  on  cardiac  physiology.  A  very 
clear  statement  of  this  theory  and  its  bearings  upon  the 
functions  of  the  auricles  will  be  found  in  some  '  Lectures 
on  the  Physiology  of  the  Vascular  System,'  by  Mayo  Collier, 
published  1888. 

But  although  the  physiological  side  of  this  question  has  for 
so  many  years  been  clearly  stated,  the  new  views  as  to  ventri- 
cular aspiration  do  not  seem  to  havo  been  generally  adopted 
by  chnicians,  and  the  necessary  modifications  in  the  theory  of 
compensation  in  mitral  disease  have  very  rarely  been  faced 
in  the  literature  of  the  present  day. 

Amongst  the  exceptions  must  be  mentioned  the  name  of 
Sir  Clifford  AUbutt,  who  accepts  the  theory  in  his  '  System 
of  Medicine.' 

The  new  theory  seems  to  be  much  more  satisfactory  than 
the  old  for  many  reasons.     It  is  more  satisfactory  to  believe 

^  Read  before  the  Clinical  Society  of  London,  December  13,  1901,  and 
printed  in  vol.  xxxv.  of  their  Transactions. 

412 


IN  MITRAL  DISEASE  413 

that  the  strong  left  ventricle  is  able  to  compensate  for  its  own 
deficiencies  instead  of  having  to  fall  back  for  assistance,  as  the 
old  theory  would  have  us  beheve,  upon  the  w-eak  right  side  of 
the  heart,  or  the  still  weaker  pulmonary  capillaries.  Also  from 
chnical  and  pathological  standpoints  it  proves  more  satisfactory 
than  the  old  one,  and  I  have  adopted  it  as  a  w^orking  hypothesis 
for  the  last  seventeen  years,  and  have  not  yet  found  it  to  be 
at  fault. 

The  facts  brought  forward  in  this  essay  are  the  outcome 
of  an  investigation  into  the  loudness  of  the  heart  sounds  in 
health  and  in  valvular  disease,  but  more  especially  as  regards 
the  loudness  of  the  second  cardiac  sound  in  the  pulmonary 
area. 

According  to  the  old  or  vis  a  tergo  theory  of  compensation, 
the  pulmonary  second  sound  ought  to  be  always  more  or  less 
accentuated  in  mitral  disease,  because  a  very  considerable 
portion  of  the  work  of  compensation  is  supposed  to  rest  upon 
the  right  ventricle.  According  to  the  new  or  vis  a  fronte 
theory,  almost  the  entire  w^ork  of  compensation  is  done  by  the 
left  ventricle  itself,  owing  to  an  increase  in  its  aspiratory 
power,  and,  therefore,  according  to  this  theory,  when  compen- 
sation is  good  the  right  ventricle  wiU  have  no  extra  work  to 
do,  and  the  pulmonary  second  sound  will  be  of  normal  loudness. 

The  result  of  my  observations  points  unmistakably  towards 
•  the  accuracy  of  the  latter  or  vis  a  fronte  theory. 

For  the  purpose  of  measuring  the  heart  sounds,  I  found, 
after  many  experiments  in  obliteration  of  the  heart  sounds  by 
the  interposition  between  the  stethoscope  and  the  chest  wall 
of  disks  of  rubber,  felt,  sponge,  &c.,  that  the  simplest  and  best 
method  was  to  use  a  bag  of  air  for  cutting  off  the  heart  sounds. 
To  do  this  an  empty  thin-walled,  elastic  rubber  bag  (a  deflated 
toy  balloon)  is  placed  between  the  chest -piece  of  a  binaural 
stethoscope  and  the  chest  wall,  and  by  its  inflation  the  stetho- 
scope is  slowly  lifted  up  until  the  heart  sounds  are  no  longer 
heard.  The  height  to  wdiich  the  particular  sound  is  audible 
is  measured  by  means  of  a  small  platform,  placed  between 
the  stethoscope  and  the  bag,  which  slides  up  and  down  on  thi'ee 
legs,  which  are  graduated  in  fractions  of  an  inch,  and  upon 
which  can  easily  be  read  off  the  height  of  the  chest-piece  of  the 


414  THEORY  OF  COMPENSATION 

stethoscope  when  the  sounds  are  lost .  The  inflation  can  be  done 
by  the  mouth  through  a  rubber  tube,  which  can  be  compressed 
by  the  lips  or  teeth  when  it  is  desired  to  maintain  the  fullness 
of  the  bag  for  a  time.  Very  exact  measurements  can  be  quickly 
made  by  this  apparatus.  In  the  statistics  wliich  follow,  I  have 
adopted  yq  inch  as  the  standard  for  measuring  the  distance  to 
which  the  sounds  are  audible,  and  in  speaking  of  the  loudness 
of  the  sound,  I  shall  only  give  the  number  of  sixteenths  of  an 
inch  at  which  it  is  still  audible — e.g.  a  sound  whose  loudness 
I  call  '  sixteen '  is  one  audible  1  inch  away  from  the  chest 
wall  with  the  apparatus  used.  A  sound  of  '  twenty-four  '  is 
one  audible  1|-  inches  away. 

The  observations  I  have  made  have  shown  that  this  method 
of  measmingthe  sounds  is  most  reliable,  and,  moreover, removes 
some  sources  of  fallacy.  It  enables  the  hstener  to  distinguish 
between  an  accentuation  of  the  second  sound  due  to  real  increase 
in  the  loudness  of  the  valvular  sound,  and  one  due  simply  to 
the  normal  sound  being  better  heard  owing  to  the  pulmonary 
artery  being  more  superficial  than  usual.  Also  in  several  cases 
where  there  was  apparently  well-marked  accentuation  of  the 
pulmonary  second  sound,  I  found  that  the  sound  was,  in  reality 
not  audible  for  more  than  the  usual  distance  from  the  chest  wall, 
and  therefore  could  not  be  said  to  be  accentuated.  In  these 
cases  it  was  sharper  and  more  slapping  than  normal,  but  there 
was  no  true  increase  in  its  volume,  such  as  might  be  expected 
if  the  blood  tension  in  the  pulmonary  artery  were  raised. 

I  have  recorded  the  measurements  in  sixteenths  of  an  inch, 
and  in  the  tables  at  the  end  of  this  essay  the  numbers  given 
tell  the  number  of  sixteenths  of  an  inch  from  the  chest  wall 
at  which  the  particular  sound  referred  to  is  audible. 

In  the  com'se  of  the  last  few  months,  I  have  made  over 
a  hundred  observations  of  all  the  heart  sounds  in  some  fifty 
patients  suffering  from  various  ailments ;  and  in  the  cases 
of  mitral  disease,  some  twenty-six  in  nmnber,  I  have  paid 
special  attention  to  the  pulmonary  second  sound,  making 
some  150  observations  of  the  loudness  of  this  sound  alone. 

From  these  observations  it  appears  that  the  distance  of 
audibihty  of  the  pulmonary  second  sound  varies  in  healthy 
hearts  from  ten  or  twelve  up  to  twenty  sixteenths  of  an  inch, 


IN  MITRAL  DISEASE  415 

and  that  slight  ailments  or  a  Uttle  excitement  will  increase  its 
loudness  up  to  twenty  or  twenty-four  sixteenths  or  more. 

In  anaemia  in  j^oung  women,  on  the  other  hand,  the  loudness 
of  the  pulmonary  second  sound  is  apt  to  range  much  higher. 
This  is,  no  doubt,  partly  due  to  the  very  superficial  position 
of  the  pulmonary  artery  in  these  cases,  but  there  must  also 
be  some  true  accentuation.  Amongst  some  four  or  live  cases 
which  I  have  examined,  I  have  in  one  case  recorded  a  pulmonary 
second  sound  heard  48  sixteenths  of  an  inch  from  the  chest 
waU,  and  two  others  of  44  and  36  respectively. 

In  comparison  with  these  very  loud  sounds  of  'anamia, 
heard  as  much  as  3  inches  (or  yf  inch)  away  from  the  chest 
wall,  it  is  very  striking  to  find  that  in  disease  of  the  mitral 
valve  the  pulmonary  second  sound  can  rarely  be  heard  more 
than  y^  inch  to  yg  inch  away  (i.e.  1|  inches  to  1|  inches), 
and  in  only  one  case  out  of  the  twenty-six  examined  was  the 
pulmonary  second  sound  regularly  heard  as  much  as  -y|-  inch 
away  {vide  Table  II). 

The  fact  that  there  is  no  Aery  marked  increase  in  the 
loudness  of  the  pulmonary  second  sound  during  the  process 
of  compensation  is  also  shown  in  Table  III,  wliich  shows  a  series 
of  observations  upon  a  patient  with  mitral  stenosis  with 
marked  failure  of  compensation,  who  speedily  recovered 
under  treatment,  and  in  whom  the  regular  loudness  of  the 
pulmonary  second  sound  never  exceeded  22. 

In  one  case  of  compensated  mitral  regurgitation  the  onset 
of  anaemic  dilatation  of  the  right  ventricle  was  accompanied 
by  a  rise  in  the  loudness  of  the  pulmonary  second  sound  fi-om 
16  or  18,  at  which  it  usually  stood,  to  44. 

In  another  case  a  little  nervous  excitement  caused  a  pulmo- 
nary second  sound,  usually  heard  only  16  or  20  sixteenths 
of  an  inch  away,  to  be  audible  at  a  distance  of  28  inches, 
and  once  at  40  inches. 

The  discussion  of  the  cause  of  this  low  average  in  the 
loudness  of  the  pulmonary  second  sound  would  be  out  of  place 
here ;  but  the  fact  is  interesting  as  showing  that  the  pulmonary 
second  sound  is  much  louder  is  anaemia  and  nervous  excitement 
than  it  is  when  the  right  ventricle  is  supposed  to  be  working 
at  its   hardest,  in  order  to  try  to  overcome  the  embarrass- 


416  THEORY  OF  COMPENSATION 

iiient  of  the  pulmonary  circulation  due  to  mitral  stenosis  or 
regurgitation. 

I  now  turn  to  the  theoretical  consideration  of  the  newer 
theory  of  compensation,  in  order  that  the  bearings  of  my 
observations  on  the  theory  may  be  estimated  ;  and  I  have,  for 
the  sake  of  brevity,  expressed  the  theory  in  a  series  of  pro- 
positions, some  self-evident  and  some  debatable,  and  needing 
any  support  which  my  observations  as  to  the  loudness  of  the 
heart  sounds  can  give. 

In  Mitral  Incompetence 

Proposition  I. — The  process  of  compensation  necessitates 
dilatation  of  the  cavity  of  the  left  ventricle,  as  well  as  hyper- 
trophy of  its  walls,  and  the  amount  of  dilatation  in  the  com- 
pensated heart  is  directly  proportional  to  the  amount  of 
blood  which  regurgitates  into  the  auricle  at  each  beat  of  the 
heart. 

As  mitral  incompetence  involves  the  leakage  back  into 
the  auricle  of  a  certain  part  of  the  contents  of  the  ventricle  at 
each  beat  of  the  heart,  it  therefore  follows  that  in  order  to 
compensate  for  this  leakage  and  allow  of  a  normal  amount 
being  thrown  into  the  aorta  at  each  beat — 

1.  The  ventricle  must  enlarge  so  as  to  hold  both  the 
normal  amount  and  that  which  will  escape  back  into  the 
auricle. 

2.  It  must  thicken  its  walls  so  as  to  be  able  to  move 
this  additional  volume  of  blood. 

3.  The  theory  of  the  enlargement  of  the  ventricular  cavity 
is  as  follows  :  On  the  first  occurrence  of  regurgitation  through 
the  mitral  valve  a  progressive  over-distension  of  the  auricle 
will  theoretically  result  from  the  leakage  of  blood  back  into  that 
chamber.  As  soon,  however,  as  the  size  of  the  auricle  exceeds 
that  of  the  ventricle,  the  latter  will,  during  its  expansion,  be 
drawing  towards  itself  more  blood  than  it  can  hold,  and  the 
momentum  of  the  blood  which  cannot  find  entrance  will  tend 
to  dilate  the  cavity  of  the  ventricle.  In  this  way  the  ventricle 
will  be  dilated  by  its  own  aspiratory  force  until  its  size  is 
comparable  to  that  of  the  auricle.     This  will  not  occur  until  the 


IN  MITRAL  DISEASE  ill 

ventricle  is  large  enough  to  hold  the  full  amount  of  the 
leakage  in  addition  to  its  normal  contents  {vide  Essay  XII, 
pp.  435  and  436). 

Proposition  II. — The  dilatation  and  hypertrophy,  which 
can  compensate  for  the  defective  working  of  the  left  ventricle 
during  systole,  will,  according  to  this  theory,  also  relieve  the 
auricle  from  embarrassment  duiing  diastole  by  ensuring  the 
proper  filling  of  the  ventricle. 

For  (1)  since  the  enlarged  ventricle  is  able  to  accommodate 
all  the  regurgitated  blood  in  addition  to  its  normal  contents, 
it  follows  that  it  will  be  as  easy  for  the  abnormal  amount  of 
blood  to  enter  the  abnormally  large  ventricle  as  for  the  normal 
amount  to  enter  the  normal  ventricle  ;   and 

(2)  the  increased  muscularity  of  the  enlarged  ventricle 
will  ensure  the  slight  addition  to  the  aspiratory  force  which  is 
required  to  draw  the  larger  amount  into  the  ventricle. 

Proposition  III. — Therefore,  by  the  time  the  expansion  of 
the  ventricle  has  ceased,  the  auricle  will  have  been  relieved 
of  all  the  regurgitated  blood,  and  only  the  normal  amount 
will  remain  to  be  dealt  with  by  it. 

Proposition  IV. — Therefore,  in  fully  compensated  mitral 
regurgitation,  no  extra  work  will  be  thrown  upon  the  left 
auricle,  and  there  will  be  no  embarrassment  of  the  pulmonary 
circulation  and  no  accentuation  of  the  pulmonary  second 
sound. 

In  Table  IV  are  given  the  details  of  five  cases  of  compensated 
mitral  regurgitation  :  two  of  them,  Cases  IV  and  V,  rather 
severe  cases,  and  the  others  well-marked  cases.  In  each  of 
these  it  will  be  seen  that  the  average  loudness  does  not  exceed 
17,  which  is  normal. 

Proposition  V. — Neither  would  there  be  any  dilatation  of 
the  left  auricle  unless  the  regurgitation  were  extreme. 

Since  the  systole  of  the  auricle  and  of  the  ventricle  together 
occupy  one-half  of  the  cardiac  cycle,  it  follows  that  only  one- 
half  of  the  full  volume  of  blood  will  normallv  enter  the  auricle 


418  THEORY  OF  COMPENSATION 

during  this  portion  of  tiie  cyclt".  Therefore,  there  will  be  room 
in  the  auricle  during  the  ventricular  systole  for  any  amount  of 
regurgitated  blood  up  to  one-half  of  the  total  quantity  put  into 
circulation  at  each  beat.  If,  on  the  other  hand,  the  amount 
of  regurgitation  were  to  exceed  one-half  of  the  normal  output 
of  the  ventricle  there  might  be  dilatation  of  the  auricle,  even 
when  compensation  was  fully  estabhshed. 

Proposition  VI. — According  to  this  theory  of  compensation 
there  ought  to  be  a  slight  increase  in  the  loudness  of  the  aortic 
part  of  the  second  sound,  because  the  greater  expansile  force  of 
the  hypertrophied  and  dilated  ventricle  will  induce  a  more 
powerful  recoil  of  the  blood  in  the  aorta,  and  will  result  in  a 
more  powerful  closing  and  stretching  of  the  aortic  valves 
than  in  the  case  of  the  normally  acting  ventricle. 

In  Miteal  Stenosis 

According  to  this  theory,  the  left  ventricle  increases  its 
aspiratory  power  in  order  to  facilitate  the  entry  of  blood  through 
the  narrowed  orifice,  and  so  estabhsh  compensation.  This  is 
brought  about  as  follows  : — 

Proposition  VII. — In  mitral  stenosis  the  left  ventricle 
contracts  with  greater  force  than  normal  in  order  that  the 
rebound,  both  muscular  and  elastic,  may  be  correspondingly 
increased. 

1.  An  evidence  of  this  is  the  increased  loudness  of  the 
first  sound  which  occurs  in  mitral  stenosis. 

This  is  shown  in  Table  III,  which  deals  with  Case  III.  Be- 
fore the  establishment  of  compensation  the  first  sound  is  seen 
to  be  32,  sometimes  reaching  40  ;  and  after  compensation  is 
established  it  is  22  or  over,  Avhich  is  above  the  normal. 

Very  loud  first  sounds  are  also  seen  in  Cases  \  II  and  VIII  of 
Table  V  and  Cas3  X  of  Table  VI,  which  are  severe  cases  of 
mitral  stenosis.  Also  in  Table  VI  the  first  sound  in  the 
five  cases  with  good  compensation  averages  20,  as  com- 
pared with  an  average  of  about  12  in  the  five  cases  of 
mitral  regurgitation. 


IN  MITRAL  DISEASE  419 

2.  Temporary  embarrassmunt  of  tlir  circiilatiun  is  accom- 
panied by  an  increase,  often  excessive,  in  the  loudness  of  the 
lirst  sound,  which  lessens  apjain  as  the  circulation  improves 
{vide  Tables  III  and  V). 

This  is  well  shown  in  Case  \II,  Table  V,  where  the  loudness 
of  the  first  sound  is  suddenly  increased  from  36 — a  sound 
inaudible  with  the  stethoscope  ^^r  inch  from  the  chest  wall 
if  no  conductor  be  used — to  a  sound  audible  without  the 
stethoscope  at  a  distance  of  2  feet  from  the  chest.  The 
same  increase  to  a  less  extent  is  seen  in  Cases  VIII  and  IX, 
and  is  often  noticeable. 

3.  The  increase  in  the  force  of  the  ventricular  contraction 
is  also  suggested  by  the  occm-rence  of  the  hypertrophy  of 
the  left  ventricle  which  is  not  infrequently  noticed  in  mitral 
stenosis. 

Projposition  VIII. — The  left  ventricle  alters  its  beat.  Its 
contraction  terminates  with  greater  suddenness  and  force 
than  normal.  This  concentration  of  ventricular  effort  at  the 
termination  of  the  systole  has  the  effect  of  further  increasing 
the  force  of  the  ventricular  recoil  which  immediately  follows 
the  systole,  lasting  as  it  does  only  -j-j  of  a  second. 

1.  This  is  the  explanation  of  the  sharp  and  loud  end  of 
the  first  sound  which  is  so  characteristic  of  mitral  stenosis. 

2.  The  characteristic  cardiograms  of  mitral  stenosis  often 
show  a  more  sudden  recession  of  the  heart  from  the  chest 
wall  at  the  end  of  the  systole  than  in  the  normally  beating 
heart. 

Pwposition  IX. — As  a  result  of  this  additional  aspiration, 
the  auricle  can  be  relieved  of  much,  if  not  all,  of  the  additional 
work  which  the  narrowness  of  the  mitral  valve  entails.  We 
find  very  frequently  an  absence  of  dilatation  of  the  left  auricle 
in  mitral  stenosis  in  cases  where  compensation  was  perfect  at 
the  time  of  death  {vide  Dr.  Sam  ways,  British  Medical  Journal, 
vol.  ii,  1898,  p.  365). 

Proposition  X. — Therefore,  in  compensated  mitral  stenosis, 
if  the   narrowing   be  not   very    excessive,  no   extra   work  is 


420  THEORY  OF  COMPENSATION 

thrown  upon  the  right  side  of  the  heart,  and  there  is  no  en- 
gorgement of  the  kmgs. 

1.  As  evidence  of  this,  we  find  the  pulmonary  second  sound 
of  normal  loudness,  even  in  cases  of  severe  mitral  stenosis 
{vide  Table  VI  and  Table  V,  Cases  VII  and  VIII,  in  part). 

2.  We  find  that  the  accentuation  of  the  pulmonary  second 
sound,  which  is  characteristic  of  failing  compensation,  gi-adually 
lessens  as  compensation  improves  {vide  Table  II). 

3.  We  may  find  no  clinical  evidences  of  pulmonary  congestion 
or  engorgement,  even  in  severe  cases  of  mitral  stenosis. 

Proposition  XI. — We  may  also  expect  some  increase  in  the 
loudness  of  the  aortic  second  sound,  apaii  from  that  due  to 
increased  arterial  pressure,  because  of  the  increased  ventricular 
aspiration,  as  suggested  in  Proposition  VI. 

In  conclusion,  although  I  am  not  able  to  bring  a  very  large 
number  of  observations,  owing  to  the  amount  of  time  required 
to  make  the  careful  observations  here  recorded,  I  nevertheless 
hope  that  I  have  brought  forward  enough  evidence  to  show 
the  desirability  of  maldng  wider  investigations  Avith  regard  to 
this  important  question. 

The  importance  of  this  question,  so  far  as  treatment  is 
concerned,  is  obvious  ;  for  if  the  expansion  movement  does 
play  an  important  part  in  compensation,  Ave  are  gi'eatly 
handicapped  as  regards  the  treatment  of  our  patients  by  our 
almost  entire  ignorance  as  to  the  effect  of  drugs  upon  that 
important  expansion  movement.  A  recognition  of  our  need 
of  having  cardiac  tonics  classified  into  those  which  increase 
the  expansile  force  of  the  ventricle  and  those  which  do  not 
will  be  the  first  step  tow^ards  having  that  need  supplied. 


Summary  of  the  Tables,  Showing  the  Loudness  of 
THE  Heart  Sounds  in  Health  and  in  Valvular 
Disease 

The  figures  given  show  the  distance,  in  sixteenths  of  an  inch, 
to  which  the  sound  is  audil)le  with  the  apparatus  used  (e.g. 


IN  MITRAL   DISEASE 


421 


a  pulmonary  second  sound  of  '  16  '  is  one  audible  at  1  inch 
distance ;  one  of  '  40 '  is  one  audible  at  2^  inches  from  the 
chest  wall).  The  figures  given  in  inches  and  fractions 
(e.g.  '  =  I"  ')  show  the  greatest  distance  at  which  the  sound 
is  audible  by  a  binaural  stethoscope  when  no  conductor  is 
used. 


Pulmonary  area 

Aortic 

area 

OctftiLs  of  ciiscs  suiixiHtirisGcl  in 

this  tablo 

— 

2nd 

1st 

2nd 

1st 

sound 

sound 

sound 

sound 

I.  Averages  of — • 

1         Six  normal  hearts    . 

16 

IH 

14* 

11 

1  Table  J. 

Four  normal  hearts 

10 

16 

11 

14 

Five  hearts  in  slight  anae- 

20 

26 

20 

21 

mia,  rheumatism,  &e. 

Three    cases    of    extreme 

40 

20 

19 

15 

— 

anaemia,  &c. 

11.  Cases    with    compensated 

mitral  regurgitation  (ave- 

rage loudness   [sec   Table 
IV.l)  : 

Case  II    . 

17 

12 

13 

n 

9  observationi- 

Case  III  . 

1(> 

10 

11 

m 

6 

Case  IV   . 

7 

7 

5 

6 

2 

Case  V     . 

1() 

IS 

22 

15 

5          " 

Case  VI   . 

11) 

10 

9 

6 

3 

HI.  Cases    with    compensated 

mitral  stenosis  (see  Table 

VI): 

Case  X 

10 

21 

8 

10 

4 

Case  XI 

14 

19 

8 

13 

2 

Case  XII 

19 

i     20 

23 

16 

3          ", 

Case  XIII 

13 

20 

14 

20 

2 

Case  XIV 

16 

20 

17 

23 

4 

IV.  Cases  with  failing  compen- 

sation in  mitral  stenosis  : 

Case  I 

8 

48 =r 

14 

36 

1  observation 

Case  VIII 

23 

70=1" 

8 

30 

1 

Case  VII 

24 

2  feet 

26 

48 

Case  X 

22 

44 

~ 

Table  I 

Tal)le  showing  measurements  of  the  loudness  of  the 
normal  heart  sounds  in  the  pulmonary  and  aortic  areas 
respectively. 

The  figures  given  in  this  and   the   following  tables   are 


422 


THEORY  OF  COMPENSATION 


measurements  in  sixteenths  of  an  inch  of  the  distance  from 
the  chest  wall  at  which  the  sound  is  audible  with  the  apparatus 
used.  Figures  in  parenthesis  (16)  are  distances  at  which  the 
sound  in  question  is  sometimes  heard.  Figures  in  square 
brackets  [16]  show  the  distance  at  which,  in  an  irregularly 
beating  heart,  the  sound  may  very  occasionally  be  heard. 


Pulmonary  area 

Aortic  area 

Sex 

Age 

1 

Second  sound 

Pirst  sound 

Second  sound 

First  sound 

F. 

49 

6 

16,  18 

10,  12 

16              ' 

F. 

49 

12,  9,  12 

22  (24) 

16 

20  [24] 

M. 

51 

10,  10,  12 

14,  16 

10 

12  (16) 

M. 

36 

10.  10 

16,  16 

8 

9(12) 

M. 

36 

9,  9 

16,  16,  15 

8      . 

12 

F. 

19 

16 

10,  11  (12) 

16 

12 

F. 

23 

12  (14) 

16 

14  (16) 

14  (16) 

F. 

21 

17  (22) 

15,  20  [22] 

14  (18) 

12  [18] 

M. 

34 

14 

11 

7 

4 

M. 

41 

16,  14 

12 

15 

12 

F. 

44 

16 

20 

15 

12 

F. 

23 

16  (18) 

12  (18) 

20 

12  (14) 

Average    . 

13^ 

16-2 

14-3 

12 

Table  II 


Table  showing  a  classification  of  150  observations  upon 
the  loudness  of  the  pulmonary  second  sound  in  twenty-six 
cases  of  mitral  incompetence  and  stenosis,  according  to  their 
loudness,  and  also  to  their  occurrence  in  patients  with  fully 
established  compensation,  or  in  patients  treated  for  failing 
compensation.  This  second  group  includes  observations 
made  on  patients  after  the  establishment  of  compensation. 
In  the  uncompensated  group  in  some  nine  instances  feeble 
sounds  were  due  to  feebleness  of  the  ventricle  and  not  to  the 
establishment  of  compensation.  For  the  sake  of  complete- 
ness,  I  give  in  a  second  column,  enclosed  in  brackets,   the 


IN  MITKAL  DISEASE 


423 


number  of  '  occasional '   observations  made    in    aildition    to 
the  regular  ones. 


Degree  of  loudness  measured 

Number  of  observations  uiaile 

Number  of  obscr 

ations  made 

in  sixteenths  of  an  inch 

in  fully  compensated  hearts 

in  uncompensated  hearts 

0  to    9 

4  and 

(1) 

2  and 

(1)               ' 

10  to  14 

3  and  (3) 

18  and 

(2) 

15  to  17 

11  and 

(1) 

9  and 

(2) 

18  to  1!) 

3  and 

(0) 

10  and 

(0) 

20  to  24 

4  and 

(3) 

37  and 

(19) 

25  and  over 

0  and 

(1) 

5  and 

(12) 

25  and 

(9) 

81  and 

(36) 

Table  III 

Case  J. — Measurements  of  the  loudness  of  llie  heart 
sounds  in  a  case  of  mitral  stenosis  with  extreme  dilatation  of 
the  right  ventricle  and  dropsy,  showing  the  variations  taking 
place  during  the  restoration  of  compensation. 

On  the  date  of  the  first  measurement  the  relative  cardiac 
dullness  extended  2  inches  to  the  right  of  the  sternum  in 
the  fourth  interspace,  and  the  apex  was  in  the  sixth  left 
interspace    some    5    inches    from    the    sternum — i.e.    in    the 


Pulmonary  area 

Aortic  area 

Date 

1 

Condition  of  the 
patient 

Second  sound 

First  sound 
32  (40)  [48] 

'sound       ^'^'^"-^-^ 

23,  viii 

8 

14            36  (24)  [44] 

Very  ill. 

25,  viii 

22,  22 

24  (28) 

20,  21      22  (28) 

Much  better. 

26,  viii 

20  (22)  [32] 

22  [32] 

16  (20)    28 

Improving. 

28,  viii 

16  [17] 

22 

10  (12)    22 

„ 

4,  ix 

18  [22] 

22 

16,  16      22 

„ 

4,  ix 

20 

— 

18            — 

,, 

20,  ix 

20  [22] 

24 

20            22 

Got  lip  on  the 
18th. 

29,  ix 

20,  .19':(22) 

22  (24) 

25            25 

29,  ix 

22  (24) 

23 

22            23 

29,  ix 

24 

24 

24            25 

Note. — On  23,  viii,  the  pulmonary  second  sound  seemed  loud  and  slapping, 
but  could  not  be  heard  more  than  half  an  inch  away  from  the  chest  -wall.  On 
29,  ix,  the  loudness  of  the  sounds  last  noted  was  probably  in  part  due  to 
nervousness  produced  by  a  prolonged  examination. 


424 


THEORY  OF  COMPENSATION 


anterior  axillary  line.  At  the  time  of  the  last  measurement 
the  apex  was  in  the  fifth  left  interspace,  4  inches  from  the 
sternum,  and  the  patient  was  walking  about  with  very  little 
dyspnoea. 


Measurements    of 
mitral  regurgitation. 


Table  IV 
the    cardiac    sounds    in    compensated 


Case 

Date 

Pulmonary  area 

Aortic  area 

3,  viii 

Second  sound 

First  sound 

Second 
sound 

First  sound 

GaseII,F.,set.l5 

12,  16,  24 

8,  14,  14 

9 

8 

5,  viii 

14,  20 

8,  10 

14 

2 

10,  viii 

16,  16,  18 

10,  10 

18 

6 

4,  ix 

18  (20) 

28 

10 

14 

Case  III,  M.       . 

6,  viii 

16,  14 

8,  10 

14 

8,  12,  14 

7,  viii 

12 

10 

10 

8 

10,  viii 

18,  18 

10,  12.  12 

10,  12 

14,  16 

14,  viii 

18  [22] 

9 

10 

15 

CaseIV,M.,Ee.26 

8,  viii 

4,6 

4,  6 

6 

6 

29,  viii 

10 

13 

4 

7 

Case  V,  F.,  a3t.  33 

22,  viii 

16.  141 

12 

22 

16 

5,  ix 

20  [28] 

18 

22 

14 

19,  ix 

15,  15 

24 

21 

14 

Case  VI,  F.       . 

23,  viii 

17,  18 

8 

10 

4 

■ 

26,  viii 

_ 

14  (20) 

12 

8 

8 

^  At  this  date  the  pulmonary  second  sound  seemed  much  louder  and  sharper 
than  the  aortic,  but  on  testing  it  with  the  apparatus  used  it  was  found  that 
(he  aortic  second  sound  had  more  jienetrative  power  than  the  pulmonary. 


IN  MITRAL  DISEASE 


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426    THEORY  OF  COMPENSATION  IN  MITRAL  DISEASE 


Table  VI 


Table    showing    the    loudness    of    the    heart    sounds    in 
compensated  mitral  stenosis. 


Case 

Date 

Pulmonary  area 

Aort'c  area 

Second 

First 

Second 

First 

11, 

viii 

sound 

sound 

sound 

sound 

Case  XI,  mitralsto- 

16  (20) 

20  [26] 

8 

14  [18] 

nosis  and  double 

26, 

viii 

12  (14) 

18  [20] 

8 

12  [18] 

aortic  murmur 

Case  XII,  F.,  set. 

15, 

viii 

20,  22 

16,  22 

24,  25 

20 

42 

22, 

viii 

14  [10] 

16,  22 

20 

13 

Case  XIII,  M.,  set. 

24, 

ix 

8(12) 

17 

16 

17,  very 

33,  a  severe  case 

well. 

7, 

xi 

19 

22 

12 

24,  breath 
bad.       i 

Case  XIV,  M.,  set. 

19, 

ix 

16,  16  (22) 

23 

18  (22) 

26 

40 

31, 

X 

16,  16 

18 

16  (18) 

21 

Case  X,  F.,  mitral 

3, 

viii 

8,  12 

20,  22 

8 

10 

and  aortic 

viii 

10,  12 

22 

0  (mui  - 
mur) 

10 

Case  X,  Compen-  ' 

10. 

viii 

24  (.32) 

32,28(24) 

0  (muj  - 

Murmur. 

sation     failings 

14, 

viii 

22  (28) 

44 

mur) 



again 

4, 

ix 

12  (14) 

48  (tV  in.) 

— 

— 

Essay  XII.— ON  THE  DIASTOLIC  CARDIAC  SOUND 
WHICH  CAUSES  SPURIOUS  REDUPLICATION  OF 
THE  SECOND  SOUND  AT  THE  APEX,  AND  IS 
SOMETIMES  CALLED  THE  THIRD  SOUND  OF 
THE  HEART  1 

The  object  of  this  essay  is  to  record  several  cases  in  which 
this  sound  was  well  heard,  because  I  think  they  throw  important 
light  upon  the  mode  of  occurrence  and  the  clinical  value  of 
this  diastohc  cardiac  sound. 

But  before  describing  the  cases,  I  must  discuss  briefly 
what  I  believe  to  be  the  cause  and  the  meaning  of  this  sound. 
I  take  what  I  consider  to  be  the  generally  accepted  view, 
that  this  spurious  reduplication  of  the  second  sound  is  due 
to  the  appearance  of  an  additional  sound  after  the  true  second 
sound,  and  that  this  sound  is  in  some  way  produced  by  the 
entry  of  blood  into  the  ventricle  at  the  commencement  of 
diastole.  This  view  was  ably  advocated  twenty  years  ago  by 
Dr.  Sansom,  and  is  well  supported  by  arguments  in  his  book 
on  the  '  Diagnosis  of  Diseases  of  the  Heart.'  I  need  not  speak 
of  the  chnical  features  of  this  sound  :  they  have  been  often 
described — but  nowhere,  in  my  opinion,  more  clearly  and 
accurately  than  by  Dr.  Arthur  Phear  in  the  Lancet  for  1897, 
p.  97.  With  him,  I  agree  that  so  definite  and  distinct  a  sound 
ought  to  have  a  name  of  its  own.  It  has  been  called  '  the  third 
sound  of  the  heart,'  and  I  do  not  think  a  more  appropriate 
name  could  be  found  for  it,  and  for  the  sake  of  clearness  and 
brevity  I  must  ask  to  be  allowed  to  call  it  '  the  third  sound  of 
the  heart '  in  this  essay. 

The  sound  to  which  I  refer  in  this  essay  is  a  short,  sharp 
sound.     I  do  not  refer  to  the  mitral  diastolic  murmur. 

1  Read    before  the  Clinical  Society  of  London,  November  9,   1900,  and 
printed  in  vol.  xxxiv.  of  their  Transactions. 

427 


428  THE  THIRD  SOUND 

The  theoretical  part  of  this  paper  involves  so  many  points 
upon  which  proof  may  rightly  be  asked  for,  that  I  have  found 
considerable  difficulty  in  condensing  all  I  have  to  say  into 
the  space  at  my  disposal.  The  ground  is,  in  part,  covered 
by  a  paper  upon  the  diastolic  expansion  movement  of  the 
ventricles  which  I  read  at  the  Ipswich  meeting  of  the 
British  Medical  Association  {vide  Essay  X).  For  the  sake 
of  brevity,  I  have  put  the  theoretical  part  of  my  paper  into 
the  following  series  of  propositions  : — 

1.  The  diastolic  expansion  of  the  ventricles  plays  so 
important  a  part  in  the  circulation  that  it  must  be  reckoned  as 
a  distinct  phase  of  the  cardiac  cycle  {he.  cit). 

2.  Kecord  of  the  second  cardiac  sound  on  the  cardiogram 
shows  that  this  sound  occurs  at  or  just  after  the  com- 
mencement of  this  expansion  movement  {vide  Cardiograms, 
Case  II,  figs.  1  and  2  ;  Case  V,  figs.  12  and  13  ;  and  Case  VI ; 
also  Plate  XII  at  end  of  book). 

3.  Eecord  of  the  so-called  third  sound  on  the  cardiogram, 
and  careful  measurement  of  the  heart  sounds  and  tracings 
show  that  the  third  sound  occurs  at  or  just  before  the  com- 
mencement of  the  period  of  muscular  relaxation  {vide 
Cardiograms,  Cases  III,  V,  and  VI). 

4.  Therefore  the  third  sound  of  the  heart  occurs  at  the 
end  of  the  expansion  movement,  and  marks  the  commencement 
of  the  third  phase  of  the  ventricular  cycle.  It  therefore 
resembles  the  first  and  second  sounds  in  marking  the 
commencement  of  a  distinct  phase. 

The  first  sound  occurs  at  the  commencement  of  the 
ventricular  contraction. 

The  second  sound  occurs  at  the  commencement  of  the 
ventricular  expansion. 

The  third  sound  occurs  at  the  commencement  of  the 
ventricular  relaxation. 

5.  The  duration  of  the  expansion  movement  is  usually 
about  one-tenth  of  a  second — i.e.  from  about  half  to  two- 
thirds  as  long  as  the  ventricular  systole  (see  Table  of 
Measurements  on  p.  429). 

G.  In  cases  where  the  third  sound  is  well  marked  there  is 
often  to  be  seen  in  the  cardiogram  a  short  sharp  rise,  imme- 


OF  THE  HEART 


429 


diately   following  the   fall   due  to   the  muscular  relaxation. 

This  oscillation  I  propose  to  call   (from  my  belief  as  to  its 

origin)  the  suction  recoil  wave. 

7.  This  wave  varies    somewhat  in    character  : — 

(a)  It  may  be  only  or  mainly  visible  in  tracings  taken 

at  the  apex,  and  may  be  more  or  less  due  to  a  tilt  forward 

of  the  relaxed  anterior  wall  of  the  heart,  such  as  might  be 

caused  by  the  impact  against  it  of  a  current  of  blood  entering 

the  ventricle  from  the  auricle. 

(fe)  In    other    cases    it    is    disproportionately  greater    the 

Measurements  of  Phases   of  the  Cardiac  Cycle 
Measured  in  twentieths  of  a  second. 


}              Case 

Measurements  of  sounds  i 

Measurements  of  cardiogram 

Aver- 

\ 
Aver- 

j   Case  II     .      . 

age 

age 

I  Systole  . 

3 

H 

3 

^ 

— 

— 

4 

H 

4 

H 

4-2 

1  Expansion  . 

— 

- — 

2 

— 

2 

2 

2 

li 

1-96 

Total  beat  .      . 

10 

lU 

lOi 

9J 

9 

— 

11 

11 

10 

10 

10-48 

Number  of  beats 

— 

— 

— 

7 

7 

10 

5 

measured 

Case  III 

Systole  .      .      . 

3J 

H 

— 

— 

— 

3i 

31 

4 

U 

415 

Expansion  . 

— 

2i 

2 

H 

2* 

2 

2 

2' 

2 

Total  beat  .      . 

12 

12 

12 

11 

11 

11-6 

12 

11 

lU 

11-4 

Number  of  beats 

7 

13 

6 

7 

7 

6 

11 

12 

measured 

Case  V 

Systole  . 

5 

5 

— 

— 

5 

5k 

6 

5-8 

Expansion  . 

— 

— 

2 

n 

1-8 

n 

2 

1-8 

Total  beat  .      . 

14 

12 

14 

12 

13-2 

12 

14 

13-2 

Number  of  beats 

8 

5 

.5 

4 

6 

9 

measiured 

__^. 

more  rapid  the  previous  fall  of  the  lever,  and  might  be  largely 
mechanical  or  of  the  nature  of  a  rebomid  of  the  lever.  (As 
this  rebound  does  not  occur  to  the  same  extent  in  the  normal 
heart,  or  in  simple  mitral  regurgitation,  it  seems  to  have  some 


^  The  time  between  the  first  and  second  sounds  is  reckoned  as  the  systole, 
although  the  first  sound  occurs  just  after  its  actual  commencement.  The 
time  between  the  second  and  third  sounds  gives  the  duration  of  the  expansion 
movement. 


430  THE  THIRD  SOUND 

pathological  significance,  and  to  imply  an  abnormal  excess 
of  intraventricular  tension  at  the  moment  when  it  occurs.) 

(c)  In  other  cases  this  suction  recoil  wave  is  observable  in 
tracings  taken  from  every  available  part  of  the  ventricle  wall, 
and  is  evidently  due  to  a  sudden  increase  in  the  volume  of 
the  ventricle,  such  as  could  only  occur  by  the  sudden  entry  of 
blood  with  considerable  force  {vide  Cases  II,  III,  and  IV). 

8.  In  some  cases,  therefore,  where  this  third  sound  occurs, 
we  seem  to  have  evidence  of  some  increase  of  tension  within 
the  ventricle  just  after  the  onset  of  ventricular  relaxation, 
and  sometimes  we  see  an  actual  general  expansion  of  the 
ventricle  at  this  point  of  time. 

9.  The  cardiograms  show  that  this  increase  of  tension  is 
due  to  the  preceding  activity  of  the  ventricles,  for  the  suction 
recoil  wave  is  separated  from  the  following  auricular  systole 
by  an  interval  which  varies  with  the  varying  length  of  the 
long  pause  {vide  Cases  I  and  III). 

10.  We  may  therefore  conclude  that  this  distension  of  the 
ventricle  is  due  to  the  entry  into  it  of  blood  which  was  set  in 
motion  liy  the  A'entricular  aspiration  developed  during  the 
preceding  expansion  movement.  (The  other  alternatives 
would  be  to  believe  in  a  second  ventricular  systole  in  the  middle 
of  the  long  pause,  or  to  l^elieve  in  an  early  and  wholly  un- 
precedented form  of  auricular  activity.  There  is  no  evidence 
at  all  in  favom-  of  either  of  these.) 

11.  We  therefore  can  say  that  where  the  third  sound  is 
well  marked  there  is  evidence  that  blood  is  still  flowing  into 
the  ventricle  in  a  more  or  less  powerful  stream  after  the 
relaxation  of  its  muscles  has  set  in. 

12.  It  will,  I  think,  be  readily  admitted  that  in  the  case 
of  the  normal  heart  the  size  of  the  mitral  orifice  is  so  con- 
siderable, in  comparison  with  the  cubic  capacity  of  the  auricle, 
that  a  powerful  ventricular  aspiration,  lasting  half  as  long 
as  the  systole,  would  suffice  to  draw  all  the  contents  of  the 
auricle  into  the  ventricle  by  the  time  the  aspiration  ceased. 

Therefore,  we  may  say  that  in  the  normal  heart  all  move- 
ment of  blood  due  to  ventricular  aspiration  will  practically 
have  ceased  by  the  time  relaxation  occurs. 

13.  As  a  result  of  the  above  considerations.  1  have  ad- 


OF  THE  HEART  431 

vanced  the  following  suggestions  as  to  the  mode  of  production 
of  this  sound. 

I.  The  third  sound  of  the  heart  is  not  produced  Ijy  the 
first  inrush  of  blood  into  the  ventricle.  (In  some  cases  of 
mitral  stenosis,  I  beheve  that  a  sound  or  a  murmur  may  be 
produced  at  the  mitral  orifice  by  this  first  inrush  ;  but  it  is, 
of  course,  synchronous  -with  the  second  sound.) 

II.  During  the  expansion  movement  the  segments  of  the 
mitral  valve  are,  presumably,  kept  tense  by  the  activity  of  the 
expanding  muscles,  but  on  the  onset  of  relaxation  they  are 
free  to  move.  If,  therefore,  a  sufficiently  powerful  stream  of 
blood  is  still  flowing  through  the  mitral  orifice  at  the  onset  of 
relaxation,  it  wiU  be  apt  to  move  the  valve  segments  with  an 
audible  sound  at  this  point  of  time. 

III.  If  my  view  is  correct,  the  occurrence  of  a  third  sound 
is  evidence  that  the  auricle  is  unable  to  empty  its  contents 
into  the  ventricle  as  rapidly  and  completely  as  normal. 

IV.  This  prolongation  of  the  flow  will  occur — 

(1)  Where  there  is  a  narrowing  of  the  mitral  orifice  ;   or — 

(2)  Where  the  auricle  holds  more  blood  than  the  ventricle 
can  draw  through  the  normal  mitral  orifice  during  the  expan- 
sion movement. 

V.  We  may,  therefore,  have  a  third  sound,  occurring — 

(1)  In  mitral  stenosis. 

(2)  Where  the  auricle  is  so  dilated  as  to  hold  more  blood 
than  the  ventricle  does. 

(3)  Also,  probably,  where  the  muscle  of  the  ventricle  is 
too  weak  to  develop  an  amount  of  aspiration  sufficient  to 
empty  the  auricle  as  rapidly  as  normal. 

The  cases  to  which  I  wish  to  refer  belong  mostly  to  the 
second  of  the  three  last-named  groups,  but  I  shall  first  show  two 
cardiograms  from  the  apex  of  a  case  of  ordinary  mitral  stenosis 
with  a  well-marked  third  sound.  They  both  show  (as  is  usual 
in  mitral  stenosis)  an  absence  of  any  expansion  at  the  time 
of  occurrence  of  the  second  sound  (compare  Case  V,  fig.  153). 
After  the  fall  of  the  lever  which  marks  the  onset  of  relaxation 
there  is  a  sudden  sharp  rise,  followed  by  a  second  or  a  third. 
These  are  well  marked  in  fig.  143,  which  was  taken  on  the  outer 
side  of  the  apex,  but  w^hen  the  heart  was  acting  excitedly. 


432 


THE  THIRD  SOUND 


On  this  tracing  I  did  not  record  the  heart  sounds.  I  have 
not  marked  the  position  of  the  third  sound  on  this  cardiogram, 
but  it  would  occur  at  the  foot  of  the  fall  just  before  the  recoil 


waves. 


EXPLANATION    OF    THE    PLATES 

The  tracings  here  shown  were  all  taken  with  a  Galabin's  cardiograph,  and 
are  to  be  read  from  left  to  right. 

In  all  the  tracings  except  Case  IV,  figs.  148  to  151,  and  Case  V,  fig.  154,  the 


Case  I. — Mitral  Stenosis  with  a  well-marked  Third  Sound 


Fig.    142. — Tracing  taken  at  the  Apex,  which  was   in  the   fiFTii 
Interspace,  2|  inches  from  the  Sternum. 

Record  of  the  first  aad  second  sounds  ou  the  cardiogram.  In  the  case  of  the  third  beat  the 
sound  record  is  faulty  owing  to  the  irregularity  of  the  beat.  The  third  sound  would  occur  at  or 
just  before  the  lowest  point  of  the  fall  after  the  second  sound.  The  suction  recoil  waves  following 
the  fall  are  well  shown,  and  their  relationship  to  the  long  pause  demonstrates  them  to  be  of 
ventricular  and  not  auricular  origin. 


position  of  the  cardiac  sounds  as  marked  on  the  cardiogram  was  ascertained 
by  synchronising  the  raps  of  an  electric  signal  with  the  heart  sounds,  and  in 
this  way  obtaining  a  simultaneous  record  of  the  heart  sounds  and  the  cardio- 
gram. The  actual  record  of  the  heart  sounds  is  shown  in  relation  to  the 
cardiogram  in  Case  II,  fig.  144;  Case  IV,  fig.  152;  and  in  Case  V,  fig.  153. 
In  all  other  cases  the  complete  record  is  not  shown  for  want  of  space. 

Enlarged  photographs  of  the  tracings  in  question  were,  however,  shown 
to  the  members  of  the  Society  when  this  essay  was  read  before  them,  and  the 
accuracy  of  the  interpretations  here  given  was  demonstrated. 


OF  THE  HEART 


433 


In  Case  IV,  tigs.  148  to  151,  the  theoretical  position  of  the  first,  second, 
and  third  sound  has  been  marked. 

In  Case  V,  fig.  154,  the  theoretic  position  of  the  second  sound  as  marked 
in  the  figure  was  verified  by  other  combined  tracings  from  the  same  case. 

Case  I. — Mitral  Stenosis  with  a  well-makked  Third  Sound 


Fig.  143. — Tracusu  similak  to  Fig.    142,  hut  taken  from  near  the 
Apex  and  whbk  the  Heart  was  acting  Excitedly. 


The  suction  recoil  waves  are  liigher  thau  iii  fig.  14ii 
systolic  rise  is  probably  of  auricular  origin. 


The  sharp  wave  just  before  the  uiuiu 


Case  II. — This  is  the  case  to  which  I  wish  to  draw  special 
attention  {vide  pp.  397,  407). 

It  was  the  case  of  a  girl  aged  twelve,  admitted  to  the 
Birmingham  General  Hospital  suffering  from  pericarditis 
and  rheumatic  pains,  with  a  history  of  acute  rheumatism 
eleven  weeks  previously. 

On  admission,  she  was  a  pale,  poorly  nourished  child,  with 
considerable  dyspnoea,  but  no  dropsy.  There  was  well-marked 
pericardial  friction  all  over  the  cardiac  area,  and  a  loud  mitral 
systolic  murmur,  which  was  well  conducted  to  the  axilla  and 
back.  It  w^as  specially  loud  posteriorly  in  the  left  mid-inter- 
scapular  area,  and  was  well  conducted  down  the  spinal  column, 
being  audible  as  far  as  the  sacrum.  The  apex  was,  however, 
not  displaced  outwards  or  downwards,  being  in  the  fifth  inter- 
space in  the  nipple  line.  There  was  a  loud  third  sound.  The 
aortic  valves  were  healthy.  There  was  a  slight  amount  of 
tricuspid  regurgitation  with  some  pulsation  of  the  veins  of 
the  neck,  also  some  slight  enlargement   of  the  liver,  but  no 

2   F 


434  THE  THIRD  SOUND 

pulsation.  There  was  no  marked  dilatation  of  the  heart  to  the 
right,  and  none  of  the  ordinary  signs  of  failure  of  the  right  side 
of  the  heart. 

She  remained  in  much  the  same  state  for  a  month  or 
more,  confined  to  bed  with  considerable  dyspnoea  and  marked 
ansemia.  The  increase  of  the  anaemia  was  accompanied  by 
marked  upward  dilatation  of  the  right  ventricle,  and  the  shock 

Case  II. — Mitral  Regurgitation  with  a  Well-marked  Third  Sound 
(as  well  as  the  Systolic  Murmur) 


Fig.  144. — Record  of  tSe  First  and  Second  Sounds  on  a  Cardiogram 
from  near  the  Apex.  (Taken  in  the  Fifth  Interspace,  2  inches  from 
the  Sternum.) 

Note  the  prominent  and  pointed  suction  reooil  wave  occurring  some  time  after  the  second 
sound. 


Fig.  145. — Tracing  t.\ken  from  the  Third  Left  Interspace,  1 J  inches 
FROM  the  Sternum. 

The  timing  of  the  sounds  is  not  quite  accurate.  The  positions  of  the  first  and  second  are 
recorded.  Note  the  presence  of  a  suction  recoil  wave  in  this  tracing  taken  over  the  conus 
arteriosus  of  the  right  ventricle. 

of  the  pulmonary  valve  closure  could  be  felt  high  up  in  the 
second  interspace  some  1  inch  from  the  sternum. 

After  about  five  or  six  weeks  she  began  to  show  signs  of 
ulcerative  endocarditis,  and  she  also  began  to  have  attacks  of 
anginal  pain. 

Throughout  the  case  the  symptoms  were  more  those  of 
aortic  disease  with  failing  forward  pressure  than  of  the  ordinary 
mitral  type,  and  it  was  clear  to  me  that  something  was  pre- 
venting the  ordinary  process  of  compensation  from  taking  place. 


OF  THE  HEART  435 

The  anginal  attacks  were  very  similar  to  the  ordinary  ones 
of  aortic  disease,  but  of  no  very  great  severity,  and 
not  accompanied  by  any  great  excess  of  dyspnoea,  nor  by 
the  usual  sense  of  dread.  She  gradually  got  worse,  and 
died  rather  suddenly  of  simple  cardiac  failure.  There  was 
at  no  time  any  dropsy  or  engorgement  of  veins,  nor  much 
cyanosis. 

Cardiograms  taken  from  any  part  of  the  heart  showed  an 
extremely  well-marked  suction  recoil  wave.  In  those  taken 
at  or  near  the  apex  there  was  a  sharp-pointed  wave,  just  follow- 
ing the  cessation  of  ventricular  activity,  which  rose  as  high 
as  the  systohc  eminence  itself  {vide  figs.  144  and  145).  The 
third  sound  would  come  in  the  hollow  just  before  this  recoil 
wave. 

The  diagnosis  was  that  there  was  very  considerable  mitral 
regurgitation,  ^\-ith  a  dilated  left  auricle,  because  of  the  loud- 
ness of  the  heart  sounds  in  the  interscapular  area  and  down 
the  spine  ;  also  in  view  of  the  loudness  of  the  third  sound 
(and  the  presence  of  an  occasional  diastolic  murmur)  mitral 
stenosis  was  suspected.  The  pericardium  was  probably 
adherent. 

At  the  post-mortem  there  was,  however,  no  narrowing  of  the 
mitral  orifice.  It  was  of  normal  size,  but  its  cusps  and  chordse 
were  thickened,  and  it  was  evidently  incompetent.  There 
were  recent  small  vegetations  on  the  aortic  and  mitral  valves. 
In  spite  of  the  regm-gitation  the  ventricle  was  of  normal  size, 
its  cavity  holding  90  c.c.  ;  the  left  auricle  was,  on  the  other 
hand,  very  greatly  dilated,  holding  164  c.c.  The  other  chambers 
were  not  specially  dilated. 

The  explanation  of  the  case  is,  I  believe,  as  follows  :  The 
pericarditis  preceded  the  mitral  disease,  and  the  support 
given  by  the  adhesion  of  the  pericardium  prevented  the  left 
ventricle  from  dilating  sufficiently  for  compensation  to  be- 
come established.  It  also  prevented  the  right  side  from 
faiUng,  and  therefore  great  strain  was  thrown  upon  the  left 
auricle,  causing  its  dilatation.  The  pallor,  dyspncea,  and 
absence  of  dropsy  were  due  to  the  small  amount  of  blood 
which  the  heart  could  put  in  circulation,  losing,  as  it  did,  a 
considerable  portion  of  a  normal  charge  at  each  beat,  owing 
to  the  regurgitation. 
.   This  case  gives  us  a  clear  demonstration  of  the  process  of 


436  THE  THIRD  SOUND 

compensation  when  we  read  the  clinical  signs  and  the  cardio- 
grams in  the  light  of  the  post-mortem. 

We  see  the  reason  for  the  extreme  suction  recoil  wave. 
We  have  a  ventricle  holding  only  90  c.c,  aspirating  with  all 
its  force  at  an  auricle  holding  164  c.c.  At  the  end  of  the  ex- 
pansion movement  of  the  ventricle,  when  the  ventricle  has,  in 
virtue  of  its  elastic  and  its  muscular  recoil,  drawn  all  the  blood 
into  itself  which  it  can  hold,  there  is  still  nearly  as  much 
again  in  the  auricle  waiting  to  come  in.  This  has  already 
been  set  in  motion  by  the  ventricular  aspiration,  and  its 
momentum  carries  it  on  towards  the  ventricle,  causing  its 
dilatation,  and  making  the  sudden  rise  in  the  cardiogram. 
If  the  walls  of  the  ventricle  had  not  been  unduly  resistant 
(owing  to  the  pericardial  adhesion)  this  distensile  force 
would  long  ago  have  dilated  the  ventricle  till  it  was 
large  enough  completely  to  empty  the  auricle  during 
its  expansion  movement,  and  so  re-estabUsh  normal  con- 
ditions. It  could  not  do  so,  however.  The  strong  rush 
of  l)lood  into  the  ventricle  after  the  onset  of  relaxation 
would  bt!  amply  sufficient  to  cause  the  loud  third  sound, 
heard  during  life,  and  the  prominent  recoil  wave  in  the 
cardiogram. 

This  case  has  given  me  a  clear  demonstration  of  the 
means  whereby  compensatory  dilatation  of  the  ventricle 
is  established  in  mitral  regurgitation,  and  I  feel  much 
gratitude  to  that  little  pointed  recoil  wave  in  the  cardio- 
gram. 

Case  III. — The  next  sot  of  tracings  are  from  a  child  who 
had  pericarditis,  and  whose  symptoms  were  very  similar  to 
Case  II,  but  whose  heart  was  greatly  dilated.  There  was  a 
systolic  mitral  murmur,  a  well-marked  third  sound,  and 
mid-diastolic  murmur. 

The  suction  recoil  wave  was  most  })iominent  here.  She 
probably  had  a  dilated  left  auricle,  as  in  Case  II.  She  died 
of  sudden  heart  failure,  but  unfortunately  no  post-mortem 
examination  could  be  obtained. 

In  fig.  146  the  first  and  second  sounds  are  recorded  on 
the  cardiogram,  and  in  fig.  147  the  second  and  third  sounds 
onlv. 


OF  THE  HEART 


43- 


Case  III. — Mitkal  Reguegitation  with  a  well-marked  Tuird  Sound 

The  apex  was  in  the  seveath  interspace  in  the  axillxt,  about  4}  inches  from  the  sternum. 


Fig.  146. — From  the  Sixth  Interspace,  4^  inches  from  the  Sternum 
A  record  of  first  and  second  sounds  on  the  cardiogram  is  shown.    The  suction  recoil  wave  is 

seen  after  the  diastolic  fall  of  the  lever  of  the  cardiograph. 

A  very  prominent  suction  recoil  wave  is  seen  in  tracings  taken  from  all  parts  of  the  left  and 

right  ventricles. 


J^^aound 


Fig.  147. — From  the  Seventh  Interspace  4  inches  from  the  Sternum 

(i.e.    nearly    1    INCH  internal    TO    THE   APEX    BeAT). 

Record  of  second  and  third  sounds  on  the  cardiogram  is  given.  Note  the  very  high  suction 
recoil  wave  which  follows  the  third  sound.  The  timing  of  the  third  beat  is  not  quite  accurate 
owing  to  the  irregularity  of  its  interval  after  the  preceding  beat. 


Case  1\. — The  next  set  of  tracings  are  from  a  woman,  aged 
forty-six,  who  suffered  from  palpitation,  sweUing  of  the  legs,  and 
occasional  dyspnoea.  The  interesting  feature  about  the  case 
was  that  the  third  sound  was  much  louder  than  the  first  sound. 
The  heart  was  extremely  difficult  to  time,  because  the  atten- 
tion was  at  once  arrested  hy  the  second  and  third  sounds, 
and  they  appeared  to  be  first  and  second.  There  was  a  faint 
presystolic  murmur  and  a  faint  first  sound. 


138 


THE  THIRD  SOUND 


Case  IV. — Patient  witu  a  very  Loud  Third  Hound,  a  Faint  Fikst 
Sound,  and  a  very  Faint  Presystolic  Murmur 

A  very  prominent  suction  recoil  wave  is  seen  in  tracings  taken  from  all  parts  of  tlie  left  and 
right  ventricle?. 


Fig.  148. 


Fig.  149. 


Fig.  150. 


Fig.  1.-,1 


Fig.  148. — Tracing   Taken   at  the  Apex    (in  the  Fifth  Interspace, 

4   INCHES    FROM    StERNUM). 

Fig.  149. — Tracing  Take>^  in  the  Fourth  Interspace,  I  inch  from 
Sternum. 

Fig.  150. — Tracing  Taken  in  the  Third  Interspace,  2i  inches  from 
Sternum. 

Fig.  151. — Tracing  Taken  in  the  Epigastrium. 

In  these  tracings  the  approximate  theoretical  position  of  the  heart  sounds  are  shov\n.  The 
position  of  the  third  sound  is  marked  by  a  broken  line. 

On  taking  cardiograms,  it  was  found  that  there  was  an  extremely 
prominent  recoil  wave.  In  some  parts  of  the  heart  it  was  the 
most  prominent  .part  of  the  cardiogram.  It  was  present  in 
all  tracings.  I  show  tracings  from  the  apex,  the  fourth  inter- 
space 1|  inches  out,  the  fifth  space  3 J  inches  out,  and  from  the 
epigastrium,  and  also  one  upon  which  I  succeeded  in  recording 
the  time  of  occurrence  of  the  first  and  second  sounds  upon  the 
cardiogram.    The  timing  is  sufficiently  accurate  to  show  that  the 


OF  THE  HEART 


439 


third  sound  would  occur  in  the  hollow  just  before  the  suction 
recoil  wave,  as  in  hg.  147.^  The  explanation  of  this  recoil  wave 
appearing  in  tracings  taken  over  the  right  ventricle  is  probably 
to  be  found  in  the  movement  of  the  interventricular  septum. 


Cask  IV 


Fig.  ];")2. — Record  of  thk  First  and  Second  Sounds  on  the 
Cardiogram. 

Note  tlie  pi-oniiiieut  .suction  recoil  wave  occurring  some  time  after  tlie  second  sound.  The 
irregularities  of  the  tracing  are  due  to  respiratory  movements  of  the  eliest. 

Case  V. — I  show  two  tracings  from  a  woman  with  compen- 
sated mitral  regurgitation  with  some  stenosis.  The  tracings 
show  the  prominent  expansion  movement  characteristic  of 
mitral  regurgitation.  There  was  also  in  this  case  a  well-marked 
third  sound,  and  a  mid-diastolic  murmur  following  it. 

In  this  case  the  third  sound  occurs  just  before  the  foot  of 
the  fall  of  the  apex  tracing,  and  its  place  is  often  marked  by 
a  small  oscillation  in  the  downstroke.  I  would  suggest,  as 
an  explanation  of  this,  the  possibihty  that  the  musculi  papil- 
lares  relax  slightly  before  the  rest  of  the  ventricle  wall,  and  so 
admit  of  the  third  sound  occurring  just  before  the  onset  of 
general  relaxation. 

Fig.  153  is  a  cardiogram  taken  just  internal  to  the  apex  with 
a  record  of  the  second  sound  marked  on  it.  It  shows  the 
systolic  depression  in  the  cardiogram,  followed  by  a  well-marked 

'  The  size  of  the  suction  recoil  wave  in  these  tracings  would  suggest  the 
possibility  of  its  bcino;  clue  to  an  extra  sj^stolo;  but  there  was  nothing  in  the 
character  of  the  sounds  to  suggest  this  and,  moreover,  the  rise  shown  in 
Case  III  is  nearly  as  great  as  in  this  one,  and  there  could  be  no  doubt  ^?  to 
the  sound  being  a  true  third  sound  in  that  instance. 


440 


THE  THIRD  SOUND 


Case  V. — Mitral  Regurgitation  and  Stenosis  with  a  well-marked 
Thitid  Sound 


Fig.  153. — Tracing  from  the  Apex,  showing  a  Record  of  the  First 
AND  Second  Sounds  on  the  Cardiogram,  and  the  Theoretical  Position 
of  the  Third  Sound  as  verified  by  other  Tracings. 


Fig.  154. — Tracing  taken  Internal  to  the  Apex  where  the  Diminution 
IN  the  Volume  of  the  Ventricle  at  the  End  of  the  Systole  causes  a 
Fall  in  the  Tracing. 

The  position  of  the  second  sound  is  shown  and  the  rise  due  to  tlio  diastoho  ex^iansion 
movement  is  seen.    The  tliird  sound  would  occur  in  the  following  notch. 


OF  THE  HEAKT 


441 


expansion  wave.     The  second  sound  occurs  near  the  top  of  this 
wave. 


Case  VI.  —  Anemic 
Dilatation  of  the 
Heart     with     a 

WELL-MARKED    ThIRD 

Sound 


Case  VII  shows  a  cardiogram  from  a  case  of  anaemia  with 
a  well-marked  third  sound,  and  is  a  record  of  the  second  and 
third  sounds  on  the  cardiogram.      It  shows  tlio  tliird  sound 
coinciding  with  a  small  oscillation  near 
the  foot  of  the  diastolic  fall  of  the  tracing. 

Before  concluding  this  essa5%  I  must 
express  my  indebtedness  to  my  house- 
physician,  Dr.  Cyril  Lewis,  whose 
patience  and  skill  in  manipulating  the 
cardiograph  while  my  attention  was 
taken  up  in  recording  the  heart  sounds, 
has  rendered  it  possible  for  me  to  obtain 
the  satisfactory  combined  tracings  which 
I  figure  in  this  essay. 

In  conclusion,  I  am  conscious  of 
the  difficulty  in  a  short  essay  of 
adequately  and  briefly  justif^dng  the 
theoretical  considerations  which  I  sub- 
mit, but  of  which  1  have  what  I 
consider  abundant  proof.  Nevertheless, 
the  facts  of  Case  II  speak  for  them- 
selves, and  tell  us  much  as  to  the 
conditions  which  determine  the  appear- 
ance of  this  third  sound  of  the  heart. 

In  spite  of  its  shortcomings,  I  hope  that  the  clinical 
research  which  I  have  laid  before  you  may  tend  to  an 
increase  of  our  knowledge  upon  this  most  important  but 
difficult  subject  of  the  expansion  movement  of  the 
ventricles. 


FROM  THE  Apex  show- 

FNO    A    RkcORD    of    THE 

Second      and     Third 
Sounds. 

A  slight  broail  suction 
recoil  wave  is  seen  foUowinr,' 
tho  third  ?oiiiul. 


Essay  XIII.— ON  THE  CONDUCTION  OE  THE  MITEAL 
SYSTOLIC  MUKMUK  DOWN  THE  SPINE  :  ITS 
DIAGNOSTIC  AND  PKOGNOSTIC  VALUE  i 

That  mitral  regurgitation  is  characterised  by  a  murmur 
audible  at  the  apex  and  conducted  outwards  into  the  axiUa  and 
round  to  the  angle  of  the  scapula  is  as  well  known  as  any  fact  in 
clinical  medicine  ;  but  it  is  not,  I  think,  so  generally  recognised 
that  this  murmur  is  often  audible  over  the  spines  of  the  dorsal 
and  lumbar  vertebrae,  and  may  even  be  conducted  down- 
wards into  the  pelvic  bpnes.  I  therefore  propose  in  this  essay 
to  draw  attention  to  this  physical  sign. 

The  reason  for  the  conduction  of  the  mitral  systolic  murnmr 
towards  the  axilla  is  given  somewhat  differently  by  different 
authors.  There  can,  I  think,  be  little  doubt  that  at  least  two 
factors  are  at  work  :  first,  the  conduction  of  the  murmur 
along  the  ribs  and  chest  wall,  against  which  the  apex  of  the 
heart  is  pressed  during  systole;  and  second,  and  most  im- 
portant, the  conduction  of  the  cardiac  murmur  through  the 
layer  of  lung  tissue  which  separates  the  left  ventricle  from  the 
lateral  chest  wall.  The  greater  the  hypertrophy  and  dilatation 
of  the  left  ventricle  the  thinner  will  this  layer  of  lung  become 
and  the  more  easily  will  the  murmur  reach  the  lateral  and  the 
posterior  chest  wall. 

Conduction  of  the  Cardiac  Sounds  to  the  Back 

Neither  of  these  reasons  suffice  to  explain  the  loud  conduc- 
tion of  this  murmur  down  the  vertebral  column,  which  can  be 
observed  in  a  well-marked  case  of  mitral  regurgitation.  The 
conduction  of  the  mitral  systolic  murmur  down  the   spine   is 

1  Read  before  the    Queen's  College  Medical    Society  and  printed  in  the 
Birmingliarn  Medical  Review,  October  1900. 

442 


CONDUCTION  OF  MITRAL  SYSTOLIC   MURMUR     443 

due  to  the  anatomical  relationship  of  the  left  auricle  and  left 
ventricle  to  the  bodies  of  the  vertebrae. 

On  carefully  studying  the  conduction  of  the  cardiac  sounds 
and  murmurs  over  the  posterior  chest  wall,  it  can  sometimes  be 
recognised  that  they  are  especially  well  heard  in  the  left  mid- 
interscapular  region  over  a  small  area  about  one  inch  or 
more  in  diameter  just  to  the  left  of  the  spine,  opposite  the 
fourth  and  hfth  dorsal  spines.  For  making  this  observation 
a  phonendoscope  or  similar  powerful  stethoscope  is  often 
needed. 

Relationship  of  the  Heart  to  the  Vertebk^ 

The  audition  of  the  cardiac  sounds  over  this  area  is,  no 
doubt,  due  to  the  proximity  of  the  heart  to  the  chest  wall. 
Under  normal  circumstances,  the  lung  tissue  wdiich  intervenes 
is  sufficient  to  prevent  the  cardiac  somids  from  being  conducted 
to  the  back.  AVlien,  however,  the  left  auricle  and  left  ventricle 
are  dilated,  they  push  the  posterior  margins  of  the  lungs  aside 
and  come  into  more  or  less  intimate  contact  with  the  bodies  of 
the  vertebrfB  and  the  posterior  chest  wall.  This  may  be  easily 
demonstrated  post-mortem  in  a  case  of  dilatation  of  the  left 
auricle,  by  distending  the  heart  with  hard  paraffin  prior  to  its 
removal  from  the  body.  On  removing  the  heart  after  the 
paraffin  has  been  allow'ed  to  cool  and  harden,  it  will  not  infre- 
quently be  found  that  there  is  a  distinct  groove  on  the  posterior 
aspect  of  the  auricle,  showing  where  it  was  pressed  against  the 
bodies  of  the  vertebrse.  Since  bone  is  a  good  conductor  of 
sounds  this  intimate  contact  of  the  dilated  amicle  with  the 
vertebral  column  will  ensure  that  any  sounds  which  may  be 
produced  in  the  auricle  during  its  period  of  distension,  will  be 
well  conducted  down  the  spine — ^in  just  the  same  way  as  the 
tracheal  sounds  are  often  so  well  conducted  by  the  cervical 
vertebrae  to  the  back  of  the  neck  and  the  occiput. 

These  conditions  occur  in  the  case  of  mitral  incompetence, 
for  the  regurgitating  blood  distends  the  auricle  while  the  murmur 
is  being  produced.  Further,  since  the  axis  of  the  left  ventricle 
is  directed  somewhat  backwards  as  well  as  upwards,  the  murmur- 
producing  stream  of  blood,   on  escaping  through  the  leaky 


444       CONDUCTION  OF  MITRAL  SYSTOLIC  MURMUR 

valve,  will  impinge  upon  that  part  of  the  auricular  wall  which 
is  in  most  intimate  contact  with  the  vertebraB,  and  thus  favour 
its  conduction  through  them. 

Clinical  Value  of  this  Sign 

We  are  now  in  a  position  to  make  some  estimate  of  the  value 
of  this  sign  of  which  we  are  speaking.  In  the  first  place,  we  can 
assert  that  the  conduction  of  a  mitral  systolic  murmur  to  the 
back  through  the  bones  of  the  spinal  column  is  evidence  that 
there  is  a  considerable  amount  of  mitral  regurgitation,  and 
ceteris  paribus,  the  extent  to  which  the  murmur  is  conducted 
downwards  is  a  fairly  reliable  index  of  the  extent  of  the 
regurgitation. 

We  may  also  consider  that  the  loud  audition  of  cardiac 
sounds  in  the  left  interscapular  area  and  over  the  vertebrae,  is 
distinctly  suggestive  of  the  presence  of  dilatation  of  the  left 
auricle  and  left  ventricle. 

Diagnostic  Value 

The  conduction  of  the  cardiac  sounds  to  the  interscapular 
area  affords  us  very  material  help  in  the,  at  times,  difficult  task 
of  distinguishing  between  a  mitral  and  a  tricuspid  mmmm*.  I 
have  often  known  the  diagnosis  in  such  a  case  to  be  satisfac- 
torily cleared  up  by  hearing  the  heart  sounds  pure  and  free 
from  murmur  in  the  interscapular  area  by  means  of  a  phonendo- 
scope.  As  the  left  ventricle  and  left  auricle  come  into  closer 
relationship  with  the  vertebrae  than  the  rest  of  the  heart,  a 
systohc  murmur,  if  arising  in  the  left  ventricle,  is  sure  to  be 
heard  at  the  back,  if  the  cardiac  sounds  can  be  heard  there  with 
any  degree  of  clearness.  The  reverse  of  this  does  not  hold  true, 
because  the  mitral  systolic  murmnr  is  not  the  only  one  that  is 
conducted  to  the  back. 

The  aortic  systolic  mmmur  is  conducted  along  the  hne  of  the 
aorta,  but  it  is  more  loudly  heard  over  the  upper  part  of  dorsal 
vertebrae  than  over  the  lower,  whereas  the  mitral  systohc 
murmur,  when  heard  posteriorly,  is  best  heard  near  the  fourth 
or  fifth   dorsal  spines,  and  rapidly  becomes  fainter  or  dis- 


DOWN  THE  SPINE  445 

appears  on  passing  upwards  towards  the  higher  dorsal  vertebrae. 
Again,  an  anemysm  of  the  descending  arch  or  thoracic  aorta 
may  give  rise  to  a  systolic  murmin-  in  the  interscapular  area. 

Tricuspid  Systolic  Murmur 

In  certain  cases  where  there  is  considerable  enlargement  of 
the  right  side  of  the  heart,  ^\ithout  any  great  corresponding 
enlargement  of  the  left  heart,  the  right  ventricle  and  right  auricle 
may  come  to  be  in  such  close  relationsliip  with  the  vertebrae 
that  a  tricuspid  systolic  murmur  is  conducted  to  the  back  in 
■  the  interscapular  area.  In  such  cases,  I  have  noticed  that  the 
murmm-  is  louder  on  the  right  side  of  the  spinal  column,  instead 
of  on  the  left,  as  in  the  case  of  the  mitral  systolic  murmm*. 
Also  there  is  not  much  likelihood  of  confusion,  because  in  cases 
where  a  tricuspid  murmur  is  conducted  to  the  interscapular  area 
the  regurgitation  is  usually  of  so  pronounced  a  type  that  there 
is  no  difficulty  in  recognising  it  in  other  ways. 

Fallacies 

We  must,  of  course,  remember  that  physical  signs  are  rarely, 
if  ever,  pathognomonic  of  any  single  condition,  and  in  the  case 
now  being  considered,  causes,  other  than  those  above  referred  to, 
may  lead  to  an  increase  in  the  loudness  of  the  cardiac  somids  or 
murmurs  as  heard  posteriorly.  Thus,  for  example,  consoUda- 
tion  of  the  lung,  which  normally  intervenes  between  the 
posterior  aspect  of  the  heart  and  the  chest  wall,  may  lead  to  an 
increase  in  the  loudness  of  the  heart  sounds  at  the  back. 

Or,  again,  the  normal  cardiac  sounds  may  be  abnormally  well 
conducted  to  the  posterior  chest  wall  throuj]jh  the  interposition 
of  a  mass  of  new  growth,  as  in  a  tumour  of  the  posterior  media- 
stinum. The  same  result  may  he  produced  in  tumom-s  of  the 
anterior  mediastinum  when  the  heart  is  pressed  against  the 
vertebrae  by  the  new  growth.  In  this  case,  the  probabihty  of 
a  tumour  may  be  suggested  by  the  increased  loudness  of  the 
tracheal  breath  sound  over  the  upper  dorsal  spines,  which 
results  from  the  pressm'e  of  the  lower  end  of  the  trachea  or  the 
bronchi  against  the  bodies  of  the  vertebrae. 


446      CONDUCTION  OF  MITRAL  SYSTOLIC  MURMUR 
Cardio-eespiratory  Murmurs 

Finally,  I  must  speak  of  a  sound  which  appears  very  closely 
to  resemble  a  systolic  mitral  murmur,  and  which  may  be  very 
clearly  audible  posteriorly.  I  refer  to  the  systolic  respiratory 
puffs  which  are  not  infrequently  heard  over  the  lower  lobe  of 
the  left  lung  in  nervous  subjects  when  the  heart  is  acting 
excitedly  :  or  when  the  normal  relationship  of  the  heart  to  the 
lungs  is  disturbed  by  deformity  of  the  chest  ;  or  by  pleuro- 
pericardial  adhesions,  and  similar  conditions. 

In  the  cases  referred  to,  a  S3''stolic  sound  is  produced  which 
may  most  closely  resemble  a  systolic  intra-cardial  murmur.  It 
is  a  cardio-respiratory  sound,  due  in  some  cases  to  the  pressure 
of  the  heart  or  large  vessels  upon  the  bronchi  which  go  to  the 
lower  lobe  of  the  lung.  One  bronchus,  in  particular,  runs  close 
to  the  lateral  aspect  of  the  left  ventricle,  and  it  is,  I  think,  quite 
possible  that  it  might  be  slightly  pressed  on  by  a  dilated  and 
excitedly  acting  heart.  In  most  cases,  its  true  nature  is 
shown  by  its  variation  with  respiration.  It  is  often  only  audible 
during  inspiration,  and  is  usually  not  heard  if  the  breath  be 
held.  Cases  are,  however,  by  no  means  uncommon,  where 
this  spurious  murmur  continues  even  when  the  breath  is  held, 
and  then  the  resemblance  to  an  intra-cardial  murmur  is  very 
close. 

The  points  of  diagnostic  importance  are — that  the  point 
of  maximum  intensity  of  this  sound  is  usually  not  at  the  apex  of 
the  heart.  It  may  be  an  inch  or  so  external  to  the  apex,  or  the 
sound  may  be  equally  well  heard  over  a  considerable  area  in 
the  lower  axillary  region. 

The  anterior  margin  of  the  area  over  which  the  sound  is 
heard  often  comes  up  to  within  an  inch  or  so  of  the  cardiac 
area  ;  but  the  sound  is  not  well  heard  over  the  heart  itself,  as 
would  be  the  case  if  it  were  intra-cardial. 

Posterior^,  the  sound  is  sometimes  very  clearly  heard  ;  but 
instead  of  its  being  best  heard  in  the  mid-interscapular 
area,  and  well  heard  over  the  vertebrae,  it  is  heard  equally 
well  over  the  greater  part  of  the  lower  lobe,  but  especially 
below  the  angle  of  the  scapula,  and  it  is  not  heard  over  the 
vertebrae  at  all. 


DOWN  THE  SPINE  447 

Prognostic  Value 

From  what  I  have  said,  the  prognostic  value  of  the  conduc- 
tion of  the  heart  sounds  to  the  interscapular  area  and  down  the 
spine  is  evident. 

If  in  a  case  of  mitral  regurgitation  the  sound  is  not  well 
heard  in  the  interscapular  area,  and  is  not  conducted  down  the 
vertebrse  at  all,  the  prognosis  is  good,  however  loud  the  murmur 
may  be  at  the  apex.  There  cannot  be  much  regurgitation 
without  its  showing  posteriorly. 

If,  on  the  other  hand,  the  murmur  is  audible  all  down  the 
spine  to  the  lumbar  region,  the  damage  to  the  mitral  valve 
must  be  considerable,  and  the  prognosis  correspondingly  grave. 
Simple  loudness  of  the  murmur  in  the  interscapular  area  with- 
out loud  conduction  down  the  spine  is  suggestive  of  a  failing 
and  dilated  left  auricle. 

In  conclusion,  I  do  not  wish  to  imply  by  what  I  have  said 
that  the  studj^  of  the  mode  of  conduction  of  the  mitral 
systolic  murmur  to  the  back  should  supplant  as  a  method  of 
precision  those  already  in  use — such  as  the  careful  estimation 
of  the  apex  beat,  the  size  of  the  heart,  and  the  general 
symptoms  of  the  case ;  but  I  am  certain  that  it  does  prove 
an  important  addition  to  our  means  of  estimating  the  amount 
of  damage  which  the  mitral  valve  has  sustained  in  cases  of 
mitral  regurgitation. 


PART  IV.— SUNDRY  ESSAYS  BEARING  UPON 
THE   DIAGNOSIS   OF   HEART   FAILURE 

Essay  XIV.— THE  DIAGNOSTIC  AND  PROGNOSTIC 
MPORTANCE  OF  PALLOR  AS  A  SYMPTOM  OF 
HEART  DISEASE  AND  HEART  FAILURE  ^ 

In  the  following  essay,  I  wish  to  draw  attention  to  the 
diagnostic  and  prognostic  value  of  pallor,  which  is  not  due  to 
ansemia,  when  it  occurs  as  a  symptom  of  heart  disease  and 
heart  failm'e. 

But  before  discussing  the  relationship  which  pallor  with 
out  anaemia  bears  to  heart  failure,  it  will  be  best,  in  order  to 
make  the  subject  of  this  paper  more  clear,  to  refer  briefly  to 
the  various  well-known  ways  in  which  ansemia  and  pallor  ma}^ 
be  associated  Avitli  cardiac  failure  and  disease. 

I.  The  relationship  of  anaemia  to  cardiac  disease  may  be 
purely  accidental,  as  when  a  patient  with  some  form  of  heart 
disease  becomes  angemic  through  loss  of  blood  from  gastric 
ulcer  or  other  cause,  unconnected  with  the  heart.  To  this  I 
need  refer  no  further. 

II.  Angemia  may  be  the  cause  of  the  cardiac  failure, 
as  is  seen  in  the  breathlessness  of  the  ordinary  anaemia  and 
chlorosis  which  occurs  in  adolescence,  and  also,  in  part,  in 
so-called  pernicious  anaemia. 

In  these  cases  of  anaemia,  the  clinical  evidence  is  clear  that 
the  due  circulation  of  the  anaemic  blood  through  the  lungs  does 
— for  some  cause  or  another — necessitate  the  maintenance 
of  a  great  increase  m  the  blood  pressm-e  in  the  pulmonary 
artery,  and,  consequently,  increased  power  on  the  part  of  the 
right  ventricle.  Li  proof  of  this,  it  is  only  necessary  to  poiiat 
to  the  greatly  increased  loudness  of  the  pulmonary  second 

^  Read  before  the  Birmingham  Branch  of  tlio  British  Medical  Association, 
March  11,  1908. 

448 


PALLOR  AS  A  SYMPTOM  OF  HEART  FAILURE       149 

sound.  This  increase  in  the  blood  pressure  in  the  right 
ventricle  and  pulmonary  artery,  does,  in  these  cases,  often 
exceed  the  resisting  power  of  the  thin  part  of  the  anterior  wall 
of  the  right  ventricle  and  the  so-called  conus  arteriosus,  leading 
to  their  giving  way  and  becoming  dilated.  This  dilatation. 
as  already  described  in  Essay  I,  is  evidenced  by  increased 
cardiac  dullness  and  pulsation  in  the  third  and  second  left 
interspaces  and  by  a  systolic  murmur  arising  in  the  aneurysm- 
like  dilatation  of  the  pulmonary  artery,  which  the  raised  blood 
pressure  produces  by  the  over-distension  of  its  relaxed  walls. 

III.  Ansemia  may  be  concomitant  with  the  heart  disease 
and  due  to  the  same  agency. 

For  instance,  in  ulcerative  endocarditis,  the  aneemia  is 
the  result  of  the  toxaemia  and  blood  destruction,  which  cha- 
racterises the  disease,  and  is  due  to  the  same  morbid  process 
as  the  endocarditis.  Similar^,  in  systemic  infection  by  the 
diplococcus  rheumaticus — such  as  is  seen  in  rheumatic  pneu- 
monia— both  the  anaemia  and  the  cardiac  damage  result  from 
the  activities  of  the  same  micro-organism. 

IV.  Anaemia  may  be  truly  symptomatic  —  and  result 
directly  from  the  faulty  condition  of  the  heart  and  circula- 
tion. I  need  not  dwell  long  upon  this  subject,  as  its 
importance  is  too  well  known  to  the  profession,  although,  in 
practice,  the  value  of  iron  in  the  treatment  of  heart  disease — 
especially  chronic  valvular  disease — is  sometimes  forgotten. 

One  of  the  most  potent  agents  in  producmg  anaemia  in 
heart  disease  is  the  digestive  failure,  which  results  from  the 
faulty  circulation  in  the  stomach  and  intestines,  &c.  It  is, 
therefore,  acknowledged  that  careful  attention  to  the  diet 
and  digestive  organs  is  a  very  important  part  of  the  routine 
treatment  of  heart  disease.  Good  nutrition  for  the  heart  is  in 
such  a  case  of  far  more  value  than  stimulants  ;  and  the  danger 
of  over-stimulation,  when  the  blood  is  of  poor  nutritive  value, 
must  always  be  borne  in  mind. 

When  present,  then,  anaemia  must  be  treated  energetically, 
for  its  presence  is  doubly  damaging  to  the  heart.  Firstly,  by 
interfering  with  the  proper  supply  of  food  and  oxygen  to  the 


450  PALLOK  AS  A  SYMPTOM 

heart  muscle,  and  secondly,  because  the  circulation  of  the 
anaemic  blood  through  the  lungs  throws  additional  strain 
upon  a  right  ventricle  already  fully  burdened  by  its  endeavour 
to  supplement  the  faulty  action  of  the  left  ventricle. 

In  ansemia,  therefore,  complicating  heart  disease,  iron,  in 
some  form,  will  often  prove  a  far  more  valuable  restorative  than 
the  drugs  which  we  class  as  cardiac  tonics  pure  and  simple. 

With  these  preliminary  remarks  upon  anaemia,  I  now  come 
to  the  main  subject  of  this  communication — namely,  the  occur- 
rence of  pallor  of  the  face,  &c.,  without  any  marked  anaemia, 
as  a  symptom  of  cardiac  disease  and  cardiac  failure.  For  the 
sake  of  brevity  and  for  want  of  a  better  word,  I  wish  to  use  the 
word  '  pallor  '  in  a  limited  and  restricted  sense  in  the  remainder 
of  this  essay — namely,  for  paleness  due  to  deficient  circulation 
and  not  that  due  to  a  deficiency  in  the  colouring  matter  of 
the  blood,  of  which  I  have  already  spoken,  under  the  term 
anaemia. 

Pallor  in  Transient  Heart  Weakness 

Pallor,  apart  from  anaemia,  is  an  important  sign  of  faulty 
action  of  the  heart,  and  in  its  most  extreme  and  simplest  form 
is  seen  in  an  ordinary  faint. 

In  syncope,  there  is  no  doubt  as  to  the  cause  of  the  sudden 
pallor  of  the  face,  with  its  as  sudden  return  of  colour  when  the 
cardiac  action  regains  its  normal  force. 

Here,  the  blanching  of  the  face  may  be  due  sivi'ply  to 
deficiency  of  circulating  blood  ;  but,  more  probabl}^  is  also  of 
vasomotor  origin,  and  due  to  a  contraction  of  the  superficial 
blood-vessels,  whereby  the  maximal  amount  of  the  feebly 
circulating  blood  may  be  diverted  from  the  skin  to  the  brain. 

Pallor  in  Continuous  Heart  Weakness 

In  the  more  chronic  cases  of  heart  wealmess,  there  may  be 
pallor  of  the  face,  due  to  continuing  feebleness  of  the  circulation, 
which  closely  resembles,  in  its  nature,  the  acuter  pallor  of 
cardiac  syncope.  But  its  true  cause  may  escape  recognition, 
and  the  cardiac  weakness,  which  is  really  due  to  affection  of 
the  myocardium,  may  be  mistaken    for  wealmess  secondary 


OF  HEART  FAILURE  451 

to  anaBiiiia.  The  pallor  may  bu  considered  to  be  the  cause  of 
the  cardiac  weakness  instead  of  its  result.  In  such  a  case  as 
this,  the  physical  examination  of  the  chest  would  help  to  clear 
up  the  diagnosis.  If  true  anaemia  were  the  cause  of  the  weak- 
ness, there  would,  if  the  patient  were  young,  almost  certainly 
be  some  dilatation  of  the  right  ventricle  upwards  and  to  the 
left,  and  also  increased  loudness  of  the  pulmonary  second 
sound  and  other  signs  of  a  labouring  right  ventricle.  If,  on  the 
other  hand,  the  paleness  of  the  face  were  a  symptom  of  the 
weak  heart  and  not  its  cause,  there  would  be  a  diminution  in 
the  area  of  cardiac  dullness,  weakness  of  the  cardiac  sounds, 
and,  in  all  probability,  a  high  diaphi-agm  as  well.  In  addition, 
there  might  also  be  a  marked  diminution  in  the  area  of  the 
liver  dullness,  from  shrinkage  of  the  organ,  owing  to  emptiness 
of  its  blood-vessels. 

In  speaking  thus,  I  do  not  mean  to  imply  that  pallor  is  a 
necessary  symptom  of  myocardial  weakness — at  all  events,  in 
adult  life — because,  in  many  instances,  the  colour  of  the  face 
may  be  quite  good,  in  spite  of  much  myocardial  weakness. 
Pallor,  nevertheless,  is,  when  present,  an  important  guide  as  to 
the  amount  of  myocardial  weakness  present.  It  is,  however, 
in  valvular  disease  of  the  heart  that  the  symptom  of  pallor 
affords  us  most  help  with  regard  to  the  diagnosis  and  prognosis 
of  our  cases. 

One  of  the  best  recognised  instances  of  pallor  is  that  wliicli 
occurs  in  aortic  regurgitation.  In  this  condition,  we  associate 
a  certain  patchy  paleness  of  the  face  with  the  other  signs  of  a 
severe  case,  and  we  note  that  the  greater  the  degree  of  pallor 
the  worse  is  the  prognosis. 

The  pallor  in  these  cases  is  certainly  due  (as  we  were  taught 
at  Edinburgh,  by  Professor  Grainger  Stewart,  in  1881)  to  the 
failure  of  the  heart  to  maintain  the  proper  amount  of  blood  in 
circulation. 

To  make  this  clear,  1  will  go  somewhat  in  detail  into  the 
theory  of  compensation  in  valvular  disease.  Compensation  in 
aortic  regurgitation  depends  (as  was  clearly  expressed  in  1889 
by  Dr.  Davis  in  his  '  Circulation  of  Blood  through  Diseased 
Hearts  ')  upon  two  physical  changes  in  the  ventricle. 

Firstly,  it  must  enlarge  so  that  it  can  hold  the  normal 


452  PALLOR  AS  A  8YMPT0:\[ 

amount  of  blooil  Avhich  has  to  pass  on  into  the  circulation, 
in  addition  to  tho  amount  wliifli  Avill  leak  back  out  of  the 
aorta  into  the  ventrick'. 

Thus,  if  th(^  normal  charge  )w  8  ounces  and  there  be  a  |-ounce 
leakage  at  each  beat,  the  ventricle  must  enlarge  so  as  to  hold 
rather  more  than  3J  ounces,  so  as  to  admit  of  the  3  ounces 
going  forward  and  the  J  ounce  leaking  ])ack. 

And,  secondly,  its  muscular  wall  must  hypertrophy,  so  as 
to  be  able  to  throw  this  additional  amount  of  blood  into  the 
aorta,  as  well  as  face  the  additional  strain  which  the  leakage 
causes. 

If,  howe^'er,  the  full  amount  of  dilatation  and  liypertrophy, 
which  is  necessary  for  compensation,  cannot  take  place,  owing 
to  the  extreme  amount  of  the  regurgitation,  or  from  some  other 
cause,  then  the  proper  circulation  cannot  be  carried  on  ;  for 
even  when  the  nearest  approach  to  compensation  has  been 
attained,  there  will  still  be  a  deficiency  in  the  amount  of  blood 
maintained  in  the  circulation  with  each  beat  of  the  heart ;  the 
arteries  will  be  badly  filled  and  pallor  of  the  face  wdll  result. 

In  failing  compensation  in  aortic  disease,  pallor  of  this 
nature  is  of  frequent  occurrence. 

In  the  case  of  disease  of  the  mitral  valve,  pallor,  as  distinct 
from  ansemia,  is  not  so  frequent  a  symptom  as  in  aortic  disease, 
and  its  true  importance  is  far  more  apt  to  be  overlooked 
when  it  is  present. 

The  explanation,  in  mitral  regurgitation,  however,  is  the 
same  as  in  aortic  regurgitation — namely,  that  the  left  ven- 
tricle is,  for  some  reason  or  other,  prevented  from  enlarging 
sufficiently  to  hold  the  amount  of  blood  needed  for  the  delivery 
of  the  normal  volume  into  the  aorta  at  each  beat,  in  addition 
to  what  leaks  back  into  the  auricle. 

Thus,  with  a  leakage  of  1  ounce  at  each  beat,  if  the  ventricle 
can  only  enlarge  enough  to  hold  3|  ounces  instead  of  4  ounces, 
there  will  be  a  shortage  of  |  ounce  at  each  beat,  and  the  arteries 
will  be  badly  filled  and  pallor  will  result. 

In  such  a  case  compensation  cannot  be  complete,  and 
the  patient  will  suffer  more  or  less  from  pallor  due  to  badly 
filled  arteries.  The  commonest  cause  of  such  a  failure  is 
when  the  ventricular  wall  is  undulj''  resistant,  owdng  to  an 


OF  HEART  FAILURE  453 

attack  of  adhesive  pericarditis  piiou  to  tiie  occurrence  of  the 
mitral  regurgitation.  Or,  in  cases  of  endocarditis,  occurrin^^ 
late  in  life,  when  the  cardiac  tissues  have  become  less  easily 
dilatable  than  they  are  prior  to  forty-live  or  hfty. 

These  cases,  where  pallor  is  due  to  incomplete  compensation, 
are  not  very  infrequent,  and  the  cause  of  the  pallor  is  very 
apt  to  be  overlooked,  with  the  result  that,  in  all  probability, 
too  good  a  prognosis  is  given,  and  also  the  proper  treatment 
is  not  adopted.  For,  although  the  treatment  is  apt  to  be 
tedious,  nnicli  can  be  done  for  these  cases  bj^  persistent  care, 
if  once  the  true  nature  of  the  case  is  diagnosed,  and,  in  cases 
where  adherent  pericardium  is  the  cause,  cardiolysis  may  be 
indicated  and  give  material  relief. 

We  can  all,  doubtless,  recall  cases  where  we  have  been 
able  to  get  the  patient  a  certain  distance  along  the  road  to 
recovery,  from  what  was  apparently  a  fairly  simple  mitral 
regurgitation,  and  then  all  our  efforts  seemed  to  fail  to  get 
the  patient  any  farther. 

We  were,  perhaps,  siruck  by  the  amount  of  anaemia  present, 
and  felt  that  our  efforts  must  be  directed  to  cure  that  ;  and 
therefore  we  did  our  best,  by  careful  dieting  and  the  free  use 
of  iron  and  other  hsemathiics,  to  combat  this  symptom — but 
all  to  no  pm'pose,  the  ansemia  remained  as  obstinate  as  ever. 

It  was  so  evident  that  we  did  not  think  of  making  a  blood 
count  ;  but  had  we  done  so,  we  should  probabh'  have  been 
surprised  to  tind  that  the  result  gave  a  far  better  percentage 
of  corpuscles  and  haemoglobin  than  we  expected. 

The  careful  examination  of  such  a  case  would  probably 
brmg  out  the  following  facts  : — 

There  was  a  loud  mitral  systolic  murmur,  conducted  to  the 
axilla  and  heard  very  clearl}^  in  the  interscapular  area  (over 
the  site  of  the  left  am'icle)  and  conducted  loudly  down  the 
vertebral  column  to  the  sacrum,  and.  perhaps,  audible  even 
over,  the  great  trochanter  of  the  femur — suggesting  a  very 
considerable  amount  of  regm-gitation  and  also  a  considerable 
degree  of  dilatation  of  the  left  auricle— which  might  even  be 
evident  on  percussion  in  the  left  interscapular  area. 

In  spite  of  these  evidences  of  copious  regurgitation,  we 
should  be  surprised  to  find  that  the  apex  l)eat  was  only  displaced 


454  PALLOR  AS  A  SYMPTOM 

outwards  and  downwards  to  a  very  moderate  extent, 
pointing  to  but  little  dilatation  and  hypertrophy  of  the  left 
ventricle. 

If  the  patient  had  not  passed  middle  age,  and  especially 
if  adolescence  had  not  been  passed,  a  careful  search  for  signs 
of  adherent  pericardium  in  such  a  case  as  I  am  now  describing, 
Avould,  in  all  prol)ability,  give  positive  results,  and  there  would 
be  a  suggestive  amount  of  systolic  retraction  in  the  epigastrium 
or  near  the  apex,  or — what  is  a  still  more  important  sign — there 
would  be  evident,  albeit  faint,  systolic  retraction  over  the  low^est 
ribs  on  the  left  side  at  the  back,  or  laterally  along  the  line  of 
the  insertion  of  the  diaphragm,  showing  that  the  diaphragm 
was  fixed  to  the  heart  by  the  adhesion  of  the  pericardium 
and  was  jerked  with  each  beat  of  the  heart.  In  such  a  case 
as  this,  I  have  been  able  to  obtain  a  fairly  perfect  cardiogram, 
from  over  the  tenth  rib  in  the  mid-dorsal  line,  some  4  or  5  inches 
away  from  the  nearest  point  of  the  cardiac  impulse. 

The  following  is  a  case  in  point  : — 

A  girl,  H.  W.,  aged  fifteen,  was  admitted  to  the  General 
Hospital  in  August  1906,  suffering  from  mitral  regurgitation 
and  stenosis  with  some  pericarditis.  After  two  months'  treat- 
ment she  had  much  improved,  but  was  still  very  breathless  on 
exertion  and  was  also  extremely  pale.  She  next  spent  three 
months  in  a  convalescent  hospital,  and  continued  to  improve 
slowly,  although  the  pallor  did  not  yield  to  treatment  at  all. 
In  February  1907,  her  condition  was  as  follows  :  Pallor 
slightly  less  but  still  a  marked  feature  of  the  case.  Heart 
extremely  dilated.  Apex  in  the  seventh  interspace  in  the 
anterior  axillary  line.  Well-marked  mitral  systolic  murmur 
audible  at  the  back  and  down  the  spine,  also  a  presystolic  and 
mid-diastolic  murmur  at  the  apex.  There  is  marked  dilatation 
upwards  and  to  the  left  of  the  right  ventricle,  with  a  loud 
pulmonary  systolic  murmur,  and  some  dilatation  of  the  right 
ventricle  to  the  right.  There  was  systolic  retraction  of  the 
epigastrium,  and  also  systolic  movement  of  the  lower  ribs  on 
the  left  side — suggesting  pericardial  adhesion. 

There  was  decided  increase  in  the  amount  of  dilatation  of  the 
right  ventricle  on  exertion. 

She  w-as  still  very  breathless  on  exertion. 

She  w^as  cautioned  to  be  very  careful  not  to  do  anything  that 


OF  HEART  FAILURE  455 

caused  dyspnoea,  and  during  the  next  twelve  months  steadily 
improved  in  every  way,  and,  by  February  1908,  was  so  much 
better  that  she  had  recommenced  work.  The  pallor  had 
greatly  lessened  ;  the  right  ventricle,  though  still  inclined  to 
dilate  on  exertion,  was  very  much  smaller. 

As  she  was  only  seventeen  years  old,  the  prognosis  was 
good  for  a  fairly  useful  heart,  if  she  continued  to  take  care. 

The  following  is  another  case,  where  pallor  was  a  marked 
feature  of  a  case  of  extreme  mitral  regm'gitation  : — 

E.  W.,  a  girl  aged  about  twenty,  admitted  to  hospital, 
suffering  from  extreme  dyspnoea,  marked  pallor  and  anginal 
attacks — such  as  are  commonly  seen  in  aortic  disease.  These 
symptoms,  together  with  a  rapidly  emptying  pulse  and  extreme 
pulsation  in  the  neck,  made  a  clinical  picture  closely  resembhng 
that  of  aortic  regurgitation.  The  pulse  had  not,  however, 
the  true  aortic  characteristics ;  the  neck  pulsation  was  venous 
and  not  arterial,  and  auscultation  showed  it  to  be  a  case  of  pure 
mitral  regurgitation  with  no  aortic  murmur.  There  was, 
however,  extreme  tricuspid  regurgitation. 

The  girl  died  in  an  anginal  attack,  shortly  after  admission. 
The  post-mortem  examination  showed  most  marked  mitral 
incompetence.  When  the  ventricle  was  full,  there  was  a  cres- 
centic  gap  I  inch  wide  by  f  inch  long.  On  distending  the  heart, 
the  left  auricle  held  480  c.c.  (or  about  16  ounces),  and  the  left 
ventricle  held  110  c.c.  (or  nearly  4  ounces).  The  right  auricle 
held  175  c.c.  (or  about  6  ounces),  and  the  right  ventriclf,  which 
was  hindered  from  enlarging  by  adhesions  of  the  pleura  to  the 
pericardium  and  to  the  chest  wall,  and  also  the  strength  of  its 
columnse  carnese,  held  only  85  c.c.  (or  under  8  ounces).  The 
pericardium  was  adherent,  but  not  lirmly  so. 

In  this  case,  the  extreme  amount  of  the  regurgitation  evi- 
dently exceeded  the  compensatory  power  of  the  left  ventricle, 
and  the  difficulty  was  further  enhanced  by  the  pericardial 
adhesions  hindering  the  enlargement  of  the  left  ventricle. 
The  dilatation  of  the  left  auricle  up  to  480  c.c.  was  eloquent 
testimony  as  to  the  inefficacy  of  any  compensation  for  the 
valvular  disease. 

There  was  al)undant  cause  for  the  emptiness  of  the  arterial 
system  and  the  pallor  which  resulted. 


15G  PALLOR  AS  A  SYMPTOM 

A  close4y  analogous  case  has  been  piiblishod  l)y  nic  in 
another  connection  : — 

The  gill,  aged  twelve,  .siiii'eietl  from  exactly  similar  symp- 
toms, and  marked  pallor  was  a  prominent  featm-e  of  her 
illness.  At  the  post-mortem,  the  pericardium  was  adherent. 
The  left  ventricle  had  not  enlarged  at  all,  holding  only 
the  normal  90  c.c,  in  spite  of  extreme  incompetence  of 
the  mitral  valve,  whereas  the  left  auricle  held  164  c.c.  {vide 
p.  43B). 

The  rigidity  of  the  heart  Vi^all,  which  may  occur  in  later 
life,  is  as  potent  as  adhesion  of  the  pericardium  in  preventing 
compensatory  dilatation  of  the  left  ventricle.  When  endo- 
carditis occurs  late  in  life,  the  prognosis  is  on  this  account 
very  grave.  I  am  indebted  to  Dr.  J.  H.  Clayton  for  the  notes 
of  a  most  characteristic  case  of  this  nature,  occurring  in  a 
patient  under  his  care. 

The  patient  was  a  gentleman,  aged  sixty- three,  who,  two 
years  ago,  was  told  by  one  of  the  leading  London  physicians 
that  his  heart  w^as  normal.  Tw-elve  months  ago — namely,  earh^ 
in  spring,  1907 — he  had  an  attack  of  illness,  which  was  thought 
to  be  influenza,  and  was  accompanied  by  a  certain  amount  of 
pneumonia.  Later  on,  he  became  extremely  pale  and  began  to 
have  dyspna?a  on  exertion.  He  consulted  the  same  phj^sician 
again,  who  found  he  had  a  systolic  mitral  murmur.  Later  on, 
when  Dr.  Clayton  saw  him,  there  was  well-marked  tricuspid 
regurgitation  with  pulsation  of  the  veins  of  the  neck,  as  well 
as  the  mitral  regurgitation. 

As  the  result  of  treatment,  the  tricuspid  regurgitation 
lessened,  though  the  murmur  persisted.  But  the  pallor  and 
the  breathlessness  remained  much  the  same. 

Iron  and  cardiac  tonics  seemed  powerless,  and  the  patient 
finally  came  to  the  conclusion  that  he  was  better  M'hen  he  did 
not  take  drugs,  but  simply  kept  quiet. 

The  pallor  was  continuously  a  most  marked  feature  of  the 
case. 

This  patient,  as  was  to  be  expected,  died  suddenly  in  a 
sj^ncopal  attack.  He  had  a  slight  attack  of  pneumonia,  and, 
thirty-six  hours  after  its  onset  and   with   a   temperature   of 


OF  HEART  FAILURE  457 

101°  v.,  he  tried  to  get  out  of  bed,  and  was  fouml  dead  on  the 
floor  of  his  room.  Such  sudden  heart  failui'e  is  most  frequent 
in  these  cases.     The  explanation  of  the  case  is  as  follows  : — 

This  man,  aged  sixty-two,  with  ligid  tibrous  tissues,  had 
an  attack  of  endocarditis,  in  the  course  of  a  febrile  attack 
(suggestive  of  some  septic  infection),  and  developed,  as  a  con- 
sequence, mitral  regurgitation.  The  inelastic  and  undilatable 
character  of  the  cardiac  tissue  prevented  compensatory  dilata- 
tion of  the  left  ventricle  from  taking  place. 

In  thinking  of  such  a  case  as  this,  the  question  arises  whether 
we  must  not  regard  the  softening  of  the  tissues  of  the  heart, 
which  occurs  in  acute  rheumatism,  as  a  merciful  provision  ;  for 
it  more  readily  enables  the  heart  to  dilate  to  a  degree  sufficient 
for  compensation  in  cases  wdiere  permanent  valvular  incompe- 
tence occurs. 

As  regards  the  treatment  of  these  cases  of  pallor, 
very  great  care  must  be  exercised  in  the  use  of  cardiac 
stimulants — ^such  as  strophanthus  and  digitalis.  The  forcible 
contraction  of  the  ventricle  is  apt  simply  to  result  in  further 
dilatation  of  the  auricle.  Nevertheless,  in  mitral  cases,  the 
careful  use  of  digitalis,  combined,  in  the  later  stages,  with 
gentle  exercise,  holds  out  the  greatest  chance  of  relief. 

In  young  patients,  very  considerable  improvement  will 
take  place  as  development  proceeds,  if  the  greatest  care  be 
taken  to  give  gentle  graduated  exercises  (short  of  fatigue  and 
of  dyspnoea),  and,  at  the  same  time,  to  maintain  the  general 
health  at  a  high  level. 

In  older  patients,  some  improvement  can  be  gained  by  care, 
but  there  is  less  probability  of  complete  compensation  ever 
being  established.  Wliere,  in  young  subjects,  there  is  certain 
evidence  of  adherent  pericardium  and  every  reason  to  believe 
in  the  soundness  of  the  myocardium  and  in  the  recuperative 
powder  of  the  heart,  the  relief  possible  by  removal  of  ribs  from 
over  the  heart,  by  the  operation  of  cardiolysis,  must  not  be 
forgotten. 

As  regards  prognosis,  it  is  important  to  remember  that, 
where  marked  pallor  not  due  to  anjemia  is  a  prominent 
symptom  in  mitral  or  aortic  regurgitation,  there  is  very  great 
risk  of  sudden  death  from  asvstole.     In  all  cases  of  marked 


158     PALLOR  AS  A  SYMPTOM   OF  HEART  FAILURE 

pallor  associated  with  aortic  regurgitation,  the  ordinary  risk  of 
sudden  death  is  enhanced  ;  and  where  the  same  marked  pallor 
is  a  symptom  of  mitral  regurgitation,  there  is  also  a  great  risk 
of  sudden  death.  If  anginal  attacks  have  already  occurred 
in  a  case  of  mitral  regurgitation  Avith  pallor,  this  risk  is  very 
great. 

The  importance  of  recognising  the  meaning  of  this  type 
of  pallor,  from  the  point  of  view  both  of  prognosis  and  treat- 
ment, is  my  excuse  for  dwelUng,  perhaps,  at  too  great  length 
upon  what  may  be  to  some  a  familiar  subject. 


Essay  XV.— SOME  LEG  PAINS  OF  CIRCULATORY 

ORIGIN 

The  '  pains  in  the  leg '  with  which  I  am  ahout  to  deal  are 
of  circulatory  origin,  commg  on  dui"ing  and  after  exertion, 
and  are  apt  to  give  rise  to  a  very  considerable  degree  of 
discomfort  and  disability  to  the  patient.  The  real  cause  of 
such  pains  is  frequently  overlooked. 

I  propose  to  discuss  the  following  types  of  leg  pains  : — 

I.  Pains  due  to  Dilatation  of  the  Deep  Veins  of  the 
Thigh. 

II.  Pains  Resulting  from  Deficient  Blood-supply  to 
the  Muscles. 

Due  to  either  :—  ■ 

1.  Weak  general  circulation  from  cardiac  asthenia  ;  or — 

2.  Some  local   interference  with  the  blood-supply  to  the 
nmscfes. 

(1)  By  arteritis   obliterans    (intermittent   claudication,  so 
called)  ; 

(2)  By  some  obscure  vasomotor  abnormality.     Either — 
(a)  Arterial  spasm  (?). 

{b)  Sluggish  vaso-dilatation  on  exertion  ("?). 


I.  Leg  Pains  due  to  Dilated  Deep  Veins  of  the  Thigh 

Under  this  heading,  I  am  dealing  with  a  type  of  pain  which 
is  extremely  common  -especially  among  working-class  women, 
old  or  young,  and  which  also  occurs  occasionally  in  those 
higher  in  the  social  scale,  but  whicli  occurs  very  rarely  in 
men. 

In  its  lesser  degrees  it  consists  simpl.y  of  the  aching  pain 
usually  associated  with  muscular  weariness.     In  its  extreme 

459 


460  LEG  PAINS 

degrees  it  is  au  almost  unbearable  pain,  which  prevents  the 
sufferer  from  taking  active  exertion  or  doing  hard  work 
without  long  periods  of  rest. 

Sometimes  the  pain  is  mistaken  for  rheumatism ;  sometimes 
it  is  hardly  felt  as  a  pain,  but  as  an  unbearable  discomfort 
associated  with  much  nervous  restlessness  and  imtabihty. 

Varicose  veins  of  the  legs  when  superficial  are  a  well-known 
occasional  cause  of  pain  ;  but  it  is,  I  thinl\.  not  so  widely  known 
that  dilatation  of  the  deep  veins  of  the  thigh  can  be  a  cause 
of  troublesome  and  even  of  incapacitating  paui  on  walking 
or  exertion. 

The  reason  why  this  cause  of  pain  has  not  obtained  that 
degree  of  recognition  which  its  frequency  and  its  importance 
deserves  is,  I  think,  largely  due  to  the  fact  that  frequently  in 
severe  cases  the  pain  or  discomfort  is  either  not  locaHsable  by 
the  patient  to  the  thigh  concerned,  or  is  apt  to  be  mistaken 
for  rheumatism,  whereas  m  the  less  severe  cases  the  patient 
does  not  refer  specially  to  it — it  is  so  constantly  present — but 
speaks  of  her  trouble  as  tir-edness  or  weariness. 

Pathology 

To  those  who  have  been  on  the  look-out  for  these  cases 
there  can  be  no  doubt  as  to  the  fact  that  defective  venous 
circulation  is  the  cause  of  the  pain,  but  it  is  not  possible  to 
feel  the  same  certainty  as  to  the  way  in  which  the  dilatation 
of  the  veins  produces  the  symptoms. 

On  anatomical  grounds  it  seems  likely  that  the  symptoms 
may  arise  from  pressm-e  on  the  nerve  trunks  by  the  dilated 
veins,  where  they  are  confined  in  the  same  sheath  of  fascia. 
Or,  again,  the  symptoms  may  be  due  to  iiTitation  of  the 
sympathetic  nerves  which  surround  the  blood-vessels. 

A  thii-d  alternative — which  I  think,  however,  can  be  dis- 
missed in  a  few  words — is  that  the  faulty  venous  circulation 
causes  a  retention  of  waste  products  in  the  muscles  and  so 
gives  rise  to  pain  and  weariness  on  exertion.  If  this  were 
the  explanation,  it  would  bring  these  cases  into  lino  with  those 
to  be  discussed  later  on.  As  the  prime  cause  of  this  condition 
it  must,  however,  be  rejected  in  favour  of  one  of  the  fu'st  two, 


OF  CIRCULATORY  ORIGIN  461 

because  the  pain  of  muscle  weariness  and  exhaustion  is,  in  my 
experience,  ahvaj's  locahsable  in  the  muscles  concerned,  and  is 
not  felt  as  a  referred  or  indefinite  pain,  as  is  so  often  the  case 
with  the  severe  thigh  pains  of  which  I  am  speaking.  It  is, 
however,  quite  likely  that  faulty  nutrition  takes  some  part 
in  causing  the  aching  thigh  pains  and  weariness  of  which  some 
patients  complahi. 

One  point  is  clear  from  the  symptoms,  and  that  is,  that  in  the 
more  troublesome  cases  the  pain  does  not  arise  in  the  ordinary 
way,  but  reaches  the  spinal  cord  tlirough  channels  not  usually 
concerned  with  the  origination  and  conduction  of  common 
sensation. 

Fortunately,  the  exact  pathology  of  the  condition  is,  from 
a  practical  point  of  view,  immaterial,  because  the  treatment  is 
the  same — these  cases  being  curable  hj  means  of  gentle  support 
applied  to  the  thigh.        ~  "" 

This  fact,  together  with  the  frequent  presence  of  dilated 
venules  in  the  skin  and  a  tendency,  in  the  more  severe  cases, 
for  the  feet  and  legs  to  swell  at  the  end  of  the  day,  makes  it 
practically  certain  that  dilatation  of  the  thigh  veins  is.  as  I 
have  said,  the  cause  of  this  condition. 

Nature  of  the  Pain  and  Discomfort 

1.  The  pain  complained  of  may  closely  resemble  the 
ordinary  aching  of  muscular  weariness,  except  that  it  comes 
on  after  an  amount  of  walking  or  standing,  which  would  not 
produce  any  discomfort  in  a  normal  limb,  and  the  pain  will 
be  located  in  the  thigh  concerned  and  especially  towards  its 
anterior  aspect. 

The  pain  is  usually  more  readily  caused  by  standing  than 
by  walking,  although  in  some  few  patients  the  reverse  is 
the  case,  pain  only  coming  on  after  such  exertion  as  going 
upstairs. 

It  varies  in  degree  from  a  simple  bearable  aching  up  to  a 
very  severe  pain. 

When  the  pain  has  once  become  severe  it  is  usual  for  it  to 
get  worse  very  rapidly  and  compel  the  cessation  of  exertion. 
The  patient  will  use  some  such  language  as  this  :    '  If  I  once 


462  LEG  PAINS 

let  it  get  bad,  I  find  I  can't  stand  another  minute,  because  it 
makes  the  pain  so  much  worse  that  it  becomes  unbearable.' 

2.  The  pain  may  not  be  localisable  to  any  particular  part 
of  the  thigh. 

Originating,  as  it  probably  does,  in  the  nerve  trunks  or  in 
sympathetic  nerves,  it  is  only  appreciated  as  an  irritation  of 
the  spinal  segment  or  segments  concerned  and  will  be  inter- 
preted in  one  of  the  ways  in  which  an  irritation,  which  does 
not  come  from  the  ordinary  sense  organs,  is  interpreted.  It 
may,  therefore,  be  felt  as  an  indefinite  pain  '  somewhere  ' 
about  the  thigh  or  hip,  but  one  which  the  patient  cannot 
localise  or  describe,  coming  on  as  an  indefinite  aching  discomfort, 
and  in  some  cases  of  such  severity  that  its  onset  is  greatly 
dreaded. 

3.  The  pain  may  be  felt  as  a  localised  *'  referred  pain  ' — a 
pain  in  some  definite  spot  distant  fi'om  the  site  of  origin,  but 
situated  in  the  special  skin  area  or  areas  which  correspond  to 
the  special  segment  of  the  cord  which  is  irritated  by  the  afferent 
impulses  coming  from  the  thigh.  Diagrams  of  these  special 
skin  areas,  as  worked  out  by  Dr.  Head  and  others,  are  now 
fahh^  common  in  medical  literatm-e. 

4.  The  nervous  irritation  may  express  itself  by  a  general 
disturbance  of  the  nervous  system,  causing  ill-defined  dis- 
comfort, which  is  sometimes  of  a  peculiarly  distressing  character. 
It  is  a  sensation  difi&cult  to  describe  to  those  who  have  not 
felt  it,  and  is  always  referred  to  by  patients  as  being  worse 
than  actual  pain.  They  will  use  such  expressions  as,  '  If  it 
were  only  a  pain,  I  could  bear  it.'  It  is  sometimes  called  a 
'  sickly  aching  pain.'  It  seems  to  have  a  more  distm'bing 
effect  upon  the  nervous  system  in  general  than  ordinary  pain 
has,  and  sometimes  seems  to  be  potent  in  inducing  that  irritable 
weakness  of  the  nervous  system  which  is  characteristic  of 
the  condition  known  as  neurasthenia,  just  as  is  the  case  with 
irritation  of  the  abdominal  sympathetic  nerves  by  neplu-optosis 
and  other  displacements. 

This  hritability  of  which  we  are  speaking  sometimes  ex- 
presses itself  in  muscular  restlessness,  either  limited  to  the  leg 
involved  by  the  venous  dilatation — as  in  the  case  of  a  woman 
aged  twenty-eight,  who  came  to  see  me  with  the  complaint 


OF  CmCULATOKY  ORIGIN  463 

that  she  '  had  the  fidgets  in  hor  left  leg  at  night  and  an  aching 
pain  in  it  which  prevented  lier  from  keeping  it  still ' — or  else 
as  that  general  muscular  restlessness  of  the  whole  body  which 
is  so  aptly  described  in  popular  parlance  as  '  an  attack  of 
the  fidgets.'  The  extraordinary  and  distressing  restlessness 
and  inability  to  remain  still  in  any  one  position  for  more  than 
a  few  seconds,  which  characterises  this  condition,  is  apt  to  come 
on  in  the  evening  when  fatigue  not  only  tends  to  increase 
the  dilatation  of  the  veins,  but  also  to  lessen  the  inhibitory 
powers  of  the  nervous  system.  While  suffering  from  sucli 
an  attack,  a  patient  will  try  to  describe  her  sensations  by 
saying,  '  Wherever  I  am,  I  cannot  rest,  but  want  to  be  some- 
where else.' 

Whenever  this  symptom  occurs  some  form  of  irritation 
of  the  spinal  cord,  through  other  than  the  ordinary  channels 
for  common  sensation,  should  be  looked  for. 

I  will  now  give  an  illustration  of  the  more  severe  type  of 
indefinite  pain  from  this  cause  :— 

A.  C,  aged  aljout  twentj^-six,  domestic  servant,  came  to  me 
complaining  of  neuralgia  in  the  left  hip,  aggravated  by  exertion. 

The  pain  was  of  a  deep-seated  character,  and  she  could 
neither  definitely  describe  it  nor  locahse  it.  All  she  could  say 
was  that  it  was  somewhere  in  the  region  of  the  great  trochanter 
and  the  anterior  aspect  of  the  hip  joint,  and  when  bad  it  was 
felt  down  the  leg  as  well.  The  pain  came  on  with  anything 
of  the  nature  of  over-exertion — whether  by  walking  or  using 
her  full  force  in  any  way  ;  she  therefore  dare  not  put  full  energy 
into  any  of  her  work.  IShe  dreaded  the  pain  coming  on,  because 
when  it  once  began  it  continued  and  prevented  her  from  doing 
anything  at  all  until  she  had  had  a  day's  rest  in  bed.  When 
the  pain  came  on  it  was  very  hard  to  bear  and  made  her 
extremely  irritable. 

It  was  supposed  that  the  pain  had  something  to  do  with  a 
fatty  tumour  of  the  left  hip  which  had  been  removed  eight  years 
ago.  She  had  pain  before  the  operation,  but  the  removal  of 
the  tumour  did  not  cure  it.  Two  months'  rest,  together  with 
cod-liver  oil,  however,  sufficed  to  cure  it  for  a  time. 

The  indefiniteness  of  the  pain,  its  distressing  and  irritating 
character,  and   its    relationship    to    exertion,    all    suggested 


464  LEG  PAINS 

Ahe   probability  that    it    was   clue    to   dilated  deep  veins   of 
the  thigh. 

This  diagnosis  was  amply  contirmed  by  the  treatment,  for 
the  use  of  properly  applied  elastic  webbing  bandages  for  leg 
I  and  thigh  entirely  relieved  her,  and,  instead  of  being  in 
constant  fear  of  the  pain,  she  was  able  to  take  long  country 
w^alks  and  do  hard  work  with  a  freedom  from  pain  which  she 
had  not  known  for  ten  vears. 
■  I  give  a  very  good  illustration  of  a  case  wdth  a  delinitely 
localised  referred  pain,  later  on,  Avhen  discussing  the 
diagnosis. 

Although  I  miglit  multiply  illustrations  of  the  various  types 
of  pain  here  referred  to,  it  is  not,  I  think,  necessary,  as  the 
cases  are,  as  a  rule,  easily  diagnosed  when  once  the  possibility 
of  their  occurrence  is  recognised  ;  for  the  condition  is,  as  I  have 
said,  an  extremely  common  one.  It  is,  moreover,  a  cause  of  a 
great  deal  of  misery  which  might  very  easily  be  prevented  if 
its  curability  by  the  simple  expedient  of  elastic  bandaging  of 
the  thigh  were  more  generally  known. 

Although  the  diagnosis  is,  as  a  rule,  quite  a  simple  matter, 
a  case  is  occasionally  met  with  where  the  true  cause  of  the 
patient's  pain  and  suffering  may  very  easily  be  overlooked. 
The  case  above  recorded  is  an  instance  of  this.  The  same 
is  true  of  those  cases  w^here  the  pain  is  referred  to  some  distant 
spot,  and  the  more  so  as  one  of  the  spots  to  which  the  pain 
may  be  referred  is  in  the  groin — a  spot  to  which  pain  is  referred 
from  many  different  situations. 

Another  reason  for  error  is  that  the  patients  may  be  so 
used  to  their  thigh  pains  that  they  do  not  think  of  speaking 
of  them.     The  following  is  such  a  case  : — 

A  lady  came  to  me  complaining  of  ill-health  and  some 
neurasthenic  symptoms  and  inability  to  do  as  much  as  others 
could  without  getting  unduly  tired.  On  being  asked  if  she 
had  any  pain  anywdiere.  she  said,  '  No,  except  indigestion ' ; 
but  when  questioned  fm'ther  as  to  whether  her  legs  ever  ached 
badly,  she  said,  '  Oh  yes,  they  always  ache  at  night  or  after 
walking  much,  but  then  everybody's  legs  do.' 

In  the  case  of  the  lady  in  question,  her  ill-health  was  almost 
entirely  due  to  her  leg  pains,  and  the  use  of  properly  applied 


OF  CIRCULATORY  ORIGIN  465 

elastic  support  to  the  legs  and  thighs  not  only  relieved  her 
of  all  her  pains,  but,  after  a  few  months'  perseverance,  they  so 
completely  restored  the  tone  of  the  vems  that  she  was  able  to 
leave  them  off  and  do  a  full  day's  shopping  with  less  sense  of 
tiredness  than  she  had  known  for  very  many  years.  In  this 
case  the  real  cause  of  her  tii-edness  and  want  of  enei'gy  might 
very  easily  have  been  overlooked. 

A  very  real  difficulty  in  diagnosis  will  sometimes  arise 
when  the  pain  is  simply  referred  to  the  groin  ;  and  it  may  be 
extremely  difficult  to  be  certain  of  its  cause,  for  many  pains 
may  be  referred  to  this  spot.  Most  difficulty  is,  however, 
likely  to  arise  in  distinguishing  between  pain  due  to  cohtis,  or 
irritable  colon,  and  pain  due  to  dilatation  of  the  deep  veins  of 
the  thigh.  I  had  two  such  cases  under  treatment  at  the  same 
time — both  in  women.  In  both,  severe  pain  in  the  left  grom 
prevented  them  from  walking  more  than  a  mile  or  so.  In  both 
there  was  extreme  tenderness  of  the  groin  on  palpation,  and 
handling  the  tender  spot  was  apt  to  cause  a  pain  lasting  for 
minutes  or  even  hours.  In  neither  could  I  make  out  any 
abdominal  symptoms  of  cohtis,  or  any  cause  for  the  pain  other 
than  dilatation  of  the  deep  veins  of  the  thigh.  The  one  case 
was  quite  cured  by  elastic  support  to  the  thigh,  and  the  other 
was  not.  The  latter  Ithen  treated  for  cohtis,  and  she  gradually 
improved.  A  year  or  two  later,  this  second  case  had  a  somewhat 
sharp  return  of  her  pain  on  walking,  and,  knowing  more  of  the 
wiles  of  catarrhal  irritability  of  the  colon  than  I  did  when 
treating  her  before,  I  examined  the  rectum  and  found  that  the 
highest  palpable  part  was  in  a  tender  and  irritable  condition, 
and  that  pressure  on  it  at  once  elicited  the  pain  in  the  left  groin 
of  which  she  complained.  The  pain  on  walking  was  largely 
due  to  the  pressure  of  a  partially  retroverted  uterus  upon  this 
sensitive  bowel.  When  the  bowel  was  free  from  irritability 
the  pressure  was  not  enough  to  cause  symptoms.  Reposition 
of  the  uterus  and  treatment  of  the  colitis  at  once  materially 
relieved  her. 

In  some  cases  the  opposite  difficulty  arises,  owing  to  pain 
having  its  origin  in  the  colon  being  referred  to-  the  legs. 

In  such  a  case  the  patient  may  complain  of  pain  felt  down 
the  backs  of  the  thighs  on  walking,  even  going  down  to  the 


466  LEG  PAINS 

toes  ;  but  careful  investigation  ^viil  conclusively  prove  it  to  be 
a  referred  pain  of  bowel  origin. 

Another  cause  of  doubt  may  arise  in  those  patients  who 
only  get  pains  in  the  thigh  on  going  uphill  or  running  up- 
stairs. This  is  probably  due  to  dilatation  of  the  veins,  but 
whatever  its  cause  it  has  been  cured  in  most  of  the  cases 
I  have  seen  by  the  use  of  elastic  thigh-supports. 

And  now  a  word  or  two  as  to  the  treatment. 

This  is  a  simple  matter  m  the  case  of  dilatation  of  the 
deeper  thigh  veins.  All  that  is  needed  is  gentle  support, 
sufficient  to  prevent  over-distension  of  the  vems,  but  yet 
insufficient  to  cause  such  pressure  on  the  vein  as  to  relieve 
its  muscular  walls  of  then*  proper  work.  Support  without 
undue  compression  will  strengthen  the  walls  of  the  vein  and 
enable  it  in  a  few  months  to  do  its  work  independently  of  any 
support,  whereas  undue  compression  of  the  vein  will  lead 
to  a  weakening  of  then  walls  from  disuse  and  render  the 
continuance  of  the  support  a  necessity. 

Although  the  pain  arises  in  the  thigh  only,  the  whole 
of  the  leg  must  be  supported.  For  the  leg  proper,  nothing  is 
better,  in  my  experience,  than  the  modern  crepe  bandage. 
There  is  not  the  same  risk  of  too  much  pressm'e  that  there  is 
with  an  elastic  webbing  bandage  or,  still  more,  with  the  elastic 
stocking.  The  support  of  the  thigh  is  a  more  difficult  problem, 
owing  to  the  tendency  of  the  bandage  to  slip  down.  I  think 
I  have  now  solved  the  problem,  and  found  a  simple  and  easy 
method  of  giving  the  necessary  elastic  support ;  but  it  is  with 
a  sense  of  extreme  want  of  originality  that  I  remember  it  was 
only  after  adopting  a  cumbersome  and  time-exacting  plan  for 
fifteen  or  twenty  years  that  I  have  within  the  last  few  years 
adopted  the  simple  and  easy  plan  I  am  about  to  describe. 

The  simplest  device  would  be  an  elastic  stocking,  but 
the  difficulty  of  getting  one  exactly  the  right  tightness  pre- 
vents its  practicability.  With,  however,  a  small  expenditure 
of  time  and  skill,  an  elastic  support  can  easily  be  made  out 
of  weak  elastic  webbing  bandage.  This  is  wound  round  the 
thigh  in  a  simple  spiral,  without  overlapping,  and  only  stretched 
enough  to  give  very  gentle  pressure — e.g.  a  12-inch  length 
ought  not  to  be  extended  to  more  than  14  inches.     TMien  the 


OF  CIRCULATORY  ORIGIN  467 

bandage  is  in  place,  from  the  knee  to  the  top  of  the  thigh, 
and  temporarily  secured  by  safely  pins,  the  patient  (in  nine- 
teen cases  out  of  twenty  it  is  a  woman)  takes  a  needle  and 
thread  and  fastens  each  turn  of  the  bandage  to  the  next  above 
it  along  a  Ihie  up  the  centre  of  the  thigh,  then  she  makes  a 
similar  line  of  stitchings  up  the  inner  and  then  up  the  outer 
side  of  the  thigh,  and  then  slips  the  support  (as  it  has  now 
become)  round  so  as  to  bring  the  back  to  the  fi'ont,  and  puts 
a  fourth  line  of  stitchings  down  what  is  now  the  front,  thus 
making  an  elastic  stocking  for  the  thigh.  Or  if  time  be  a 
consideration,  the  places  for  the  four  lines  of  fastenings  can 
be  marked  by  distinctive  marks  by  pen  or  pencil  by  the  doctor, 
and  the  marked  bandage  taken  home  and  sewn  together  by 
the  patient  at  her  leisure.  In  order  to  fasten  the  bandage  up, 
so  as  to  prevent  it  slipping  down,  a  tape  must  be  sewn  on 
down  the  front  and  also  one  down  the  hack,  with  loops  whereby 
the  bandage  may  be  suspended  from  the  corsets,  in  the  case 
of  a  woman,  or  to  a  belt  in  the  case  of  a  man,  or  it  may  be 
fixed  to  the  combinations  or  pants  respectively  and  drawn 
on  or  off  with  them.  The  front  tape  must  be  fastened  when 
in  the  erect  position,  but  the  back  tape  must  be  fastened  to 
the  back  of  the  corsets  when  the  thigh  is  fully  flexed,  so  that 
it  may  hold  the  bandage  up  when  the  patient  is  in  the  sitting 
posture. 

The  supports  should  be  put  on  first  thing  in  the  morning 
and  taken  off  last  thing  before  going  to  bed  at  night. 

If  the  elastic  support  thus  made  be  regularly  worn  for 
a  time,  it  can  gradually  be  left  off  after  two  or  three  months 
of  regular  wear,  being  onlj-  used  when  extra  exertion  of  any 
kind  is  expected.  Sometimes  only  a  few  months  is  sufficient 
to  cure  the  patient. 

II.  Leg  Pains  Due  to  Deficient  Blood-supply 

It  is  probably  within  the  experience  of  many  of  us  that 
overtired  muscles  are  liable  to  ache,  and,  also,  that  a  sudden 
strain  on  an  overtired  nuiscle  is  apt  to  give  rise  to  a  painful 
spasmodic  condition — famiharly  known  as  cramp.  Some  of 
us  have  experienced  the  sudden  cramp  which,  towards  the  end 


408  LEH  PAINS  DUE  TO 

of  a  long  September  day's  shooting,  is  apt  to  interfere  with 
our  negotiating  some  awkward  hedge,  or  impede  our  progress 
through  some  specially  well-grown  field  of  roots. 

'Co  state  this  fact  in  general  terms,  wo  can  say  that  the 
contraction  of  a  muscle  which  is  taxed  beyond  its  power  of 
nutritional  repair  is  painful,  and  that  such  a  muscle  is  liable 
to  uncontrollable  painful  spasm — i.e.  to  cramp. 

Now.  a  muscle  may  be  taxed  beyond  its  power  of  nutritional 
restoration  not  only  Ijy  excess  of  the  work  it  has  to  do,  as  in 
the  case  of  the  long  day's  shooting  or  the  long  bicycle  ride,  but 
also  through  a  deficiency  m  its  supply  of  nutrition  when  the 
work  required  is  7iot  excessive,  and  we  find  that  in  a  large  class 
of  cases  muscular  pain  does  result  from  defective  blood-supply 
to  the  muscles. 

This  symptom  of  nutritional  failure  appears  first  in  the 
leg  muscles,  and  especially  those  of  the  calf,  because  they 
have  to  bear,  in  the  act  of  walking,  a  heavier  strain  than 
is  thrown  upon  any  other  muscle  of  the  body  in  the  daily 
routine  of  life,  and  pain  in  the  calf  in  walking  is  a  much 
commoner  symptom  of  circulatory  failure  than  w^ould  be 
suspected  by  those  who  have  not  made  special  inquiry  into 
its  prevalence. 

The  following  is  a  good  instance  :  A  man,  during  a  game  of 
golf,  began  to  feel  unduly  tired  in  consequence — as  was  shown 
by  the  sequel — of  an  attack  of  haemorrhage  from  a  gastric 
ulcer.  On  bicycling  home,  he  found  that  a  sense  of  w^eakness 
and  cardiac  oppression  prevented  him  from  riding  up  the  least 
incline,  and  on  walking,  to  push  his  bicycle,  he  had  calf  weari- 
ness amounting  to  a  very  distinct,  though  not  specially  severe, 
aching  pain.  By  the  time  he  reached  home  there  was  distinct 
faintness  on  exertion. 

Here,  although  the  haemorrhage  cannot  have  amounted  to 
more  than  a  pint  or  so  and  caused  no  discomfort  or  disability 
afterwards,  it  so  weakened  the  circulation  while  it  was  in 
progress  that  it  produced  leg  pains  on  continued  exertion 
from  muscular  malnutrition. 

Leg  pains,  due  to  deficient  l)lood-supply,  may  be  due  : — 

Firstly,  to  feebleness  of  the  general  circulation — as  from 
myocardial  weakness  or  degeneration. 


DEFICIENT  BL00D-8ITPPLY  469 

Secondly,  to  some  local  iiitorferencu  with  the  blood-supply 
to  the  muscles,  either  : — 

1.  Of   an   organic   nature,   as    from    arteritis    obliterans, 
causing  the  so-called  intermittent  claudication,  or — 

2.  Due  to  some    functional    or    vasomotor    disturbance. 
Either  :  — 

(1)  As  a  part  of  a  more  or  less  general  condition  of  vaso- 
motor spasm  ;    or — 

(2)  As  a  result  of  what  appears  to  be  a  sluggishness  of  the 
vaso- dilator  mechanism,  which  is  called  into  play  on 
exertion  for  the  provision  of  the  extra  supply  of 
blood  required. 

(I)  Leg  Pains  Due  to  Feebleness  of  the  General 
Circulation 

This  sjrmptom  will  be  found  sometimes  a  valuable  guide  to 
the  presence  of  cardiac  weakness,  and  especialty  of  that  type 
of  cardiac  asthenia  wdiich  results  from  disease  or  weakness  of 
the  myocardium  ;  for  aching  pains  in  the  calves  of  the  legs  on 
exertion  is  often  well  marked  in  cases  where  the  heart  is  too 
weak  muscularly  to  keep  up  the  increased  circulation  which  is 
necessary  when  all  the  arterioles  in  the  muscles  are  dilated  by 
exertion.  That  it  is  not  more  generally  recognised  as  a 
symptom  of  myocardial  weakness  is,  I  think,  due  to  the  fact 
that  the  patient  does  not  think  of  referring  to  it.  He  will 
speak  of  being  too  weak  to  walk  far  or  too  easily  tii'ed,  and  it 
will  only  be  when  he  is  asked  to  go  into  detail  that  he  will 
volunteer  the  statement  that  ixdn  in  Ms  calves  prevents  him 
from  walking. 

The  occurrence  of  this  pain  on  exertion — a  definite  '  inter- 
mittent claudication ' — is  often  a  useful  guide  as  to  the 
condition  of  the  heart  muscle. 

For  instance  : — 

Two  patients  present  themselves  before  you  :  both  complain 
of  breathlessness  on  exertion  and  weakness  of  the  heart. 
One  is  slightly  cyanosed,  has  well-marked  venous  pulsation 
in  the  neck,  a  dilated  heart,  and  slightly  enlarged  liver  and 
anasarca  of  the  ankles  and  legs.     The  second  has  no  cyanosis ; 


i70  \.WA  PAINS  DUE  TO 

(he  face  may  liavu  a.ii  apparently  natural  colour,  there  is  no 
venous  pulsation  in  the  neck,  the  heart  area  is  smaller  than 
normal,  the  gastric  resonance  may  be  raised,  say,  to  the  upper 
border  of  the  sixth  rib  or  higher,  and  the  absolute  liver  dull- 
ness decidedh'  diminished  in  area,  probal)ly  not  reaching  to 
within  one  or  two  inches  of  the  middle  line,  nor  to  within  from 
half  to  one  inch  of  the  costal  arch,  and  there  is  no  dropsy. 

In  the  former  case  the  main  cause  of  the  failure  of  the 
circulation  is  mechanical  and  not  due  to  failure  in  the  nutrition 
or  of  the  vitality  of  the  cardiac  muscle.  It  is  a  case  of  valvular 
disease  or  of  failure  of  the  heart  from  overstrain  absolute  or 
relative. 

In  the  latter  case  it  is  a  pure  case  of  failure  of  the  cardiac 
muscle,  as  a  result  of  myocarditis,  toxcsmia,  &c.,  or  from 
failure  of  its  blood-supply  by  disease  of  the  coronary  arteries 
or  other  cause. 

In  the  former  case,  pain  in  the  legs  on  walking  will  not 
be  a  marked  symptom.  It  will  be  breathlessness  that  prevents 
the  patient  from  getting  al^out  as  freely  as  he  used  to  do. 
In  the  latter  case  breathlessness  will  certainly  prevent  the 
patient  from  going  up  hills  or  stairs  as  he  used  to  do,  but 
when  walking  on  the  level  it  will  be  aching  pains  in  his  calves 
that  will  be  most  apt  to  trouble  him. 

Two  such  cases  came  to  see  me  a  few  days  before  I  began  to 
write  this  essay.  Both  were  men  about  forty-four  ;  both  were 
engaged  in  the  manufacture  or  sale  of  alcohol ;  both  had  been 
perfectly  well,  so  far  as  they  knew,  until  a  few  months  prior  to 
their  coming  to  see  me ;  and  in  both  the  development  of  dyspnoea 
and  inabihty  to  work  was  traceable  to  an  overstrain.  The  first 
case  was  that  of  a  publican  with  aortic  regurgitation,  dilated 
heart,  and  dropsy,  who  some  twelve  months  ago  strained  him- 
self helping  to  get  some  barrels  into  his  cellar  and  had  gradually 
got  worse  since.  In  the  second  case,  one  of  myocardial  failure, 
the  man  had  first  became  conscious  of  heart  weakness  after 
having  taken  up  work  in  the  malting-room  of  a  brewery  at  which 
he  had  worked  for  many  years  in  another  capacity.  His  new 
duties  involved  the  shifting  of  heavy  bags  of  malt  and  sugar,  and 
at  this  work  he  gradually  developed  breathlessness,  Avhich 
fmally  forced  him  to  give  uj)  work  altogether. 


DEFICIENT  BL00D-8UPPLY  471 

On  examination,  his  heart  was  inegulai'  and  weak,  but  its 
area  was  markedly  diminished  in  size  and  there  was  no  murmur. 
There  was  a  shght  relative  increase  in  the  size  of  the  conus 
arteriosus  of  the  right  ventricle,  suggestive  of  the  fact  that  the 
primary  failure  was  in  the  muscles  of  the  left  ventricle,  rather 
than  the  right,  and  the  pulmonary  second  sound  was  relatively 
loud. 

The  first  case  had  no  pains  in  his  legs,  but  the  second  said  : 
'  I  don't  have  to  walk  long  before  my  legs  start  to  ache  ;  I 
should  not  like  to  walk  a  mile — if  I  could  go  that  far,'  As  soon 
as  the  pains  came  on,  he  was  forced  to  stop  and  rest,  for  they 
increased  rapidly  in  severity  if  he  continued  w^alking.  This 
symptom  is  not  an  uncommon  one,  if  it  be  looked  for ;  but 
the  patient,  as  a  rule,  does  not  seem  to  think  it  of  sufficient 
importance  to  mention  unless  he  be  asked  definitely.  I  have 
not  as  yet  a  long  enough  series  of  such  cases  to  enable  me  to  say 
what  are  the  conditions  which  determine  the  presence  or  absence 
of  this  symptom  in  cases  of  myocardial  weakness,  for  it  does  not 
appear  to  be  present  in  all  cases  :  sometimes  the  patient  only 
complains  of  undue  coldness  of  his  legs  on  exertion.  Neither 
have  I  as  j^et  met  with  a  case  where  exertion  produced  cramp 
as  it  does  in  the  next  class  of  case  to  be  described.  The  absence 
of  cramp  in  general  circulatory  weakness  is  probably  due  to 
the  fact  that  the  occurrence  of  dyspnoea  will  prevent  the 
patient  from  overtaxing  his  muscles  sufficiently  to  produce 
this  symptom. 

(II)  Leg  Pains  Due  to  Local  Interference  with  the 
Blood-supply  to  the  Muscles 

1.  From  organic  disease  of  the  arteries  supplying  them — 
intermittent  claudication. 

The  cases  of  so-called  intermittent  claudication  are  of  this 
nature.  In  them  arteritis  obliterans  causes  so  faulty  a  supph' 
of  blood  that  the  patient  may  only  be  able  to  walk  a  few 
hundred  yards  without  pain,  and  any  attempt  to  force  the 
muscles  to  continue  working  in  spite  of  the  pain  will  j-jving  on 
severe  cramp  in  them. 

These  cases  of  intermittent  claudication  have  received  some 


172  LEG  PAINS  DUE  TO 

attention  of  late  in  medical  literature.  Tlio  symptoms  are 
essentially  the  same  as  those  due  to  other  forms  of  defective 
nutrition  of  the  muscles — namely,  aching  pain  in  the  calves  and 
sometimes  also  in  the  thighs,  coming  on  after  the  patient  has 
walked  for  a  few  minutes  and  then  passing  off  at  once  after 
resting  a  minute  or  two.  In  addition  to  the  pain  there  is  often 
a  sense  of  contraction  as  if  a  tight  band  were  tied  round  the 
muscle.  Coldness  of  the  legs  is  also  a  well-marked  symptom 
and  often  increases  as  the  exercise  is  continued.  The  patient 
gets  colder  with  exercise  instead  of  warmer. 

A  sjmiptom  which  is  far  more  common  in  this  type  of 
lameness  than  in  the  others  here  referred  to,  is  the  occurrence 
of  cramp  on  exertion.  So  good  an  account  of  this  condition 
is  given  by  Dr.  Byrom  Bramwell,  in  A^ol.  V.  No.  8  of  his 
'  Clinical  Studies,'  that  I  shall  not  saj^  more  as  to  leg  pains  of 
this  type  here. 

2.  Muscular  pains  due  to  vasomotor  disturbance. — Inter- 
ference with  the  blood-supply,  through  some  defect  in  the  action 
of  the  intramuscular  arteries  of  obscm'e  origin  and  nature, 
is,  in  my  experience,  a  more  common  cause  of  leg  pains  than 
the  gross  arterial  disease  just  referred  to. 

The  symptoms  in  these  cases  are  similar  in  character  to 
those  just  mentioned — as  far  as  the  leg  pains  are  concerned ; 
although  the  arterial  supply  is  not  as  a  rule  poor  enough  to 
cause  cramp  in  the  muscles  on  exertion,  as  is  the  case  where 
there  is  arteritis  obliterans  of  the  larger  vessels. 

In  these  cases  there  are  no  signs  of  any  interference  with  the 
main  arterial  trunks.  The  pulsation  in  the  arteries  of  the 
leg  and  foot  is  good,  but,  nevertheless,  as  soon  as  the  patient 
tries  to  walk,  severe  leg  pains  come  on,  and  the  pain  is 
])roportional  to  the  amount  of  walking  done. 

(1)  In  one  class  of  case,  of  which  I  have  seen  several  ex- 
amples, the  symptoms  are  extremely  suggestive  of  vasomotor 
spasm.  There  are  attacks  of  lividity  or  of  pallor  and  coldness 
of  the  fingers  and  hands  as  in  Eeynaud's  disease,  or  there  may 
be  attacks  of  coldness  about  the  body  as  well  as  the  limbs. 

There  is  another  sjanptom  which  is  very  striking,  and  that 
is  the  occurrence  of  coldness  in  the  legs  on  exertion. 

When  the  patient  first  starts  lowalk,  the  legs  get  warmer 


DEFICIENT  BLOOD-SUPPLY  473 

as  a  result  of  the  exercise  ;  but  as  soon  as  tlio  legs  begin  to  aclu; 
they  begin  to  get  cold,  and  the  coldness  increases  the  longer 
they  walk.  In  cases  of  this  nature,  the  arterial  spasm — if 
such  it  be — is  not  confined  to  the  legs,  although  it  seems  to 
be  regularly  induced  there  by  the  functional  activity  of  the 
muscles. 

These  patients  will  complain  of  unpleasant  cold  sensations 
about  the  body  in  addition  to  the  coldness  of  hands  and  feet 
which  is  so  noticeable  a  symptom  of  the  contracted  arterioles 
due  to  an  excess  of  uric  acid  and  its  allies  in  the  blood. 

To  illustrate  this  better,  I  will  give  some  notes  of  the  best 
marked  instance  of  this  condition  which  I  have  seen. 

Eleanor  W.,  aged  thirty-one,  had  been  more  or  less  ailing 
since  she  was  fifteen  ["years  old.  At  twenty-four,  her  health 
broke  down,  and  she'Jiad  fainting  attacks  and  breathlessness, 
also  pain  in  the  limbs  and  occasional  cramp  ;  also  attacks  of 
cold  and  shivering,  in  which  her  teeth  would  chatter.  These 
last  named  often  came  on  at  night,  and  she  would  sometimes 
wake  up  in  an  attack.  She  had  much  pain  and  weariness  in 
her  legs  on  walking,  and  could  sometimes  hardly  walk  at  all. 
'J'lie  circulation  in  the  hands  was  very  bad  and  the  fingers 
used  often  to  go  dead,  and  she  suffered  very  much  with 
chilblains,  especially  as  a  child.  Alsoj  as  a  girl  of  twelve  to 
fourteen,  she  would  sometimes  have  attacks  of  cramp  and  of 
coldness  round  the  waist,  which  would  take  her  breath  away, 
and  she  used  to  have  to  go  into  shops  and  sit  down  because 
of  them  ;  but  these  attacks  only  came  on  in  cold  weather. 
She  used  to  walk  a  great  deal  as  a  girl,  but  could  never  get 
warm  while  walking. 

When  her  illness  began  at  twenty-four  years  of  age,  there 
were  marked  circulatory  disturbances  in  the  hands  ;  the  finger- 
nails came  off,  and  there  were  spots  like  the  scurvy  on  them — 
a  sort  of  hremorrhagic  erythematous  blotches,  to  judge  by 
her  account.  When  she  got  better,  after  two  years  or  so,  the 
hands  improved,  but  the  leg  pains  on  walking  did  not.  For 
four  or  five  years,  she  was  much  of  an  invalid,  with  heart  weak- 
ness and  leg  pains  and  attacks  of  coldness  about  the  body. 
She  saw  Sir  William  Broadbent,  who  is  reported  to  have 
been  puzzled  by  her  condition,  which  at  that  time — as  at 
present — somewhat  resembled  exophthalmic  goitre,  but  with 
most  of  the  cardinal  symptoms  missing. 


171  LEG  PAINS  DUE  TO 

She  went  to  Edinburgh  Koyal  Inlirniaiy,  and  was  under 
Dr.  Byrom  Bramwell,  who  gave  her  injections  of  strychnine 
and  Weir-Mitchell  treatment.  When  she  left,  she  was  very 
much  better  ;  the  muscles  were  in  splendid  condition,  she  says, 
and  she  did  more  during  the  next  twelve  months  than  she  had 
done  for  five  years.  Nevertheless,  the  leg  pains  remained,  and 
the  more  she  used  her  legs  the  more  they  ached. 

She  gradually  got  worse  again,  and  the  same  treatment  did 
not  seem  to  do  the  same  good. 

As  she  was  having  much  pain  from  dysmenorrhoea  it  seemed 
desirable  that  this  should  be  relieved,  and  she  therefore  had 
the  OS  uteri  dilated,  with  good  local  results  ;  but  she  was  much 
upset  by  the  anaesthetic,  and  when  she  left  the  hospital  her  legs 
were  so  bad  that  the  pain  came  on  after  standing  for  even  two 
or  three  minutes  and  got  worse  the  longer  she  was  on  them. 
The  pain  w^as  in  the  thigh  as  well  as  the  calves,  and  she  de- 
scribed the  sensation  as  that  of  a  tight  bandage  round  the  thick 
part  of  the  thigh,  squeezing  it  painfully  and  stopping  the 
circulation. 

She  also  got  pains  in  the  biceps  and  forearm  muscles  after 
continuous  work  such  as  sewing.  She  also  had  attacks  of  cold- 
ness of  the  hands  and  arms  accompanied  by  much  numbness, 
and  these  attacks  w^ere  often  followed  by  a  sense  of  great  heat 
accompanied  by  flushing  of  the  hands  and  aching  pain — similar 
to  the  so-called  '  hot  ache  '  which  children  experience  after 
their  hands  have  got  unduly  cold  in  winter. 

In  addition  to  these  symptoms  the  pulse  was  120  to  130, 
but  without  any  dilatation  of  the  heart  or  other  definite  abnor- 
mality of  thoracic  or  abdominal  organs.  Some  tremor  of  the 
hands  also  occurred  and  occasional  sense  of  throbbing  in  the 
neck  with  a  little  choking  sensation,  but  no  other  symptom 
of  Graves'  disease. 

For  the  last  year  or  two  she  has  been  very  slowly  improving, 
but  only  able  to  take  very  little  muscular  exertion  of  any  sort 
without  pain  ;  she  also  gets  frequent  attacks  of  coldness  of  her 
hands  and  sometimes  in  the  body. 

The  outstanding. feature  of  her  illness  is  pain  in  the  legs 
on  the  slightest  exertion— even  walking  a  few  times  across  the 
room  will  bring  it  on.  This  patient  was  further  improved  by 
brisk  exercises  of  short  duration — such  as  skipping — and  by 
taking  pituitar}^  extract. 

The  following  is  a  verv  different  case  from  the  last,  for  it 


DEFICIENT  BLOOD-SUPPLY  475 

occuirecl  in  un  appaicntly  liealthy  working'  man  inf>k'acl  uf  in  u 
neurasthenic  young  woman. 

The  patient,  a  night-watchman,  complained  of  pain  in  his 
legs  coming  on  in  the  course  of  his  rounds  and  causing  him 
to  stop  and  rest.  It  used  to  occur  in  both  legs,  but  at  the  time 
of  liis  admission  to  the  hospital  it  was  mainly  limited  to  the 
left  leg  and  thigh.  When  the  pain  comes  on  the  whole  leg  and 
thigh  go  cold  and  numb.  The  pain  goes  completely  away 
when  he  rests,  as  does  also  the  coldness,  which  gradually  passes 
away  from  above  downwards. 

There  was  no  sign  of  any  disease  in  the  arteries  of  the  legs, 
and  the  blood  pressure  was  good.  There  was  some  lividity  at 
times  of  the  hands,  and  they  were  of  a  deep  red  colour  with  very 
slow  capillary  reflux. 

(2)  Pains  due  to  defective  vaso- diktat  ion. — In  what  will,  T 
think,  prove  to  be  another  group  of  cases,  of  which  I  have  seen 
one  or  two  instances,  the  disturbance  is  hmited  to  the  legs, 
and  there  are  no  signs  of  any  general  vaso-motor  spasm  ;  but  the 
condition  seems  to  consist  in  some  persistent  interference  with 
the  supply  of  the  blood  to  the  muscles,  or  the  removal  of  waste 
products  from  them,  leading  to  premature  fatigue.  I  cannot 
say  whether  this  change  consists  of  vaso-motor  spasm  of  the 
muscular  arterioles  or  sluggishness  of  the  vaso-chlator  mechan- 
ism interfering  with  the  proper  dilatation  of  the  vessels  during 
muscular  activity^ — or  whether,  on  the  other  hand,  there  is  actual 
arteritis  or  pathological  rigidity  of  the  vessels ;  or,  further, 
the  defect  is  due  to  some  interference  with  the  removal  of  the 
lymph  from  the  muscles. 

Certainly,  in  some  cases,  the  cause  is  of  a  removable  nature, 
as  is  shown  in  the  case  subsequently  to  be  narrated. 

In  this  thh'd  group  of  cases,  where  there  is  no  evidence 
of  arterial  spasm,  the  most  hkely  explanation  is  a  sluggishness 
of  the  controlling  mechanism  when  the  muscular  arterioles 
are  dilated  in  response  to  the  call  for  the  increased  blood- 
supply  to  which  muscular  exertion  gives  rise. 

A  kind  of  '  habit  '  paresis,  similar  to  such  conditions  as 
hysterical  aphonia  and  many  other  functional  errors  of  the 
nervous  system. 


476  LEG  PAINS  DTTE  TO 

The  following  mo.st  interesting  case  appears*  to  bo  one  of 
this  nature  : — 

As  the  sufferer  is  a  doctor,  who  has  kindly  sent  me  notes 
of  his  own  case,  it  has  additional  scientific  value.  His 
experience  is  as  follows  : — 

In  November  1907,  he  began  to  have  pain  in  his  legs  and  to 
feel  unduly  tired  after  his  day's  work,  which,  while  suggestive 
of  rheumatism,  did  not  yield  to  anti-rheumatic  remedies. 

They  gradually  got  worse,  and  were  accompanied  by  sen- 
sations of  prickmg  in  the  legs  and  calves,  also  '  pins  and  needles' 
and  numbness  ;  also  there  Avere  localised  sensations  of  heat 
in  the  legs  and  a  distinct  '  girdle  '  sensation  around  the  upper 
part  of  the  calf.  These  sensations  came  on  after  walking 
half  a  mile  or  so,  and  would  soon  become  quite  unbearable  if 
walking  were  persisted  in  ;  also  there  was  such  weakness  that 
he  felt  his  legs  would  giA^e  way  under  him.  Standing  or  sitting 
for  a  minute  or  two  would  quickly  relieve  him  and  allow  of 
his  going  on  without  discomfort. 

He  remained  in  this  condition  all  through  the  winter  months 
and  had  carefully  to  avoid  much  walking.  During  the  attacks 
of  pain  and  numbness  there  was  never  any  coldness,  pallor, 
or  congi-stion  of  the  skin. 

In  April  1908,  he  consulted  Dr.  Byrom  Bramwell  in  Edin- 
burgh, who  found  that  there  was  no  noticeable  disease  or 
narrowing  of  the  main  arteries  of  the  legs,  and,  as  he  was  in 
the  habit  of  doing  much  of  his  work  on  a  motor  bicycle — to  the 
extent  of  some  100  miles  or  so  per  w^eek — he  advised  the  dis- 
continuance of  this  and  of  ordinary  bicychng,  together  with 
more  walking.  He  endeavoured  to  follow  this  advice  as  far  as 
he  could,  but  was  not  able  to  trace  any  connection  between  the 
periods  of  aggravation  and  remission  of  his  leg  pains  and  the 
use  or  non-use  of  his  motor  bicycle.  He  continued  much 
the  same  till  June,  being  quite  unable  to  walk  as  much  as  a 
mile  without  resting  to  allow  the  pains  to  pass  off. 

In  June,  he  tried  a  game  of  tennis  and  played  for  three  hours 
without  any  discomfort.  He  found  no  harm  resulted  from 
the  exercise,  and,  on  the  contrary,  there  was  decided  improve- 
ment in  his  powers  of  walking.  Since  then,  he  has  plaj^ed 
tennis  frequently  and  has  remained  very  free  from  attacks 
or  pain,  although  he  has  had  many  slight  ones ;  and  in  August, 
he   once   walked   eight    miles   without   any    discomfort.     As 


DEFICIENT  BLOOD-SUPPLY  477 

regards  the  causation  of  his  attack,  ho  thinks  the  vibration 
of  the  motor  bicycle  had  much  to  do  with  it,  and  has  noticed 
that  even  after  driving  a  motor-car  he  has  had  a  shght  attack 
of  the  pain. 

The  pathology  of  this  case  is  clear  in  so  far  that  it  shows 
the  attacks  of  pain  to  have  been  due  to  some  form  of  defective 
nutrition  of  the  muscles. 

In  this  case,  the  sudden  violent  movements  necessary  in 
playing  tennis  so  increased  the  nutritive  interchange  of  blood 
or  lymph  as  to  leave  the  circulation  in  the  muscles  permanently 
improved. 

^Vllether  the  defect  were  in  the  vaso-motor  nerves,  the 
arterioles,  venules,  or  lymphatics,  either  the  sudden  powerful* 
call  for  more  blood,  or  else  the  violent  muscular  contractions 
broke  down  the  habit  of  quiet  and  ineffective  circulation 
which  had  previously  been  established. 

This  curative  action  of  powerful  contraction  also  raises 
the  question  whether  the  attack  of  cramp  which  occurs  in 
tired  muscles  is  not  also  a  cm-ative  effort  on  nature's  part. 
The  powerful  contraction  squeezes  out  the  waste  products 
that  have  been  slowly  accumulating  and  enables  the  muscles 
once  more  to  do  their  work  effectively.  Certain  it  is  that, 
after  a  violent  attack  of  cramp  which  at  the  time  seemed 
likely  to  deprive  me  of  the  last  hour  of  a  day's  shooting,  I  have 
sometimes  been  surprised  to  find  that  I  could  go  on  walking 
more  freely  and  could  fuiish  my  day  with  no  more  return  of 
cramp. 

Also  I  remember  a  twenty-mile  bicycle  ride  after  a  long 
day's  fishing,  where  from  about  the  fifth  to  the  eighth  mile  I 
had  cramp  in  apparently  every  muscle  of  both  legs,  but  was 
able  to  ride  the  last  ten  or  twelve  miles  with  perfect  freedom 
and  enjoyment,  in  spite  of  much  of  the  road  being  uphill. 

Such  cases  as  these  just  referred  to,  open  up  a  large  field 
for  research  and  suggest  the  probability  that  the  vaso-motor 
system  is  dependent,  for  its  proper  functions,  upon  some  internal 
secretion  or  other  special  substance,  and  that  when  this  is 
deficient  in  amount  the  vaso-motor  functions  are  not  properly 
performed.  The  last  case  seems  to  suggest  the  probability 
that,  as  with  other  functions  of  the  nervous  system,  a  tem- 


478  LEG  PAINS  DUE  TO 

porary  failuro  of  function  may  be  perpetuated  as  a  '  habit 
paralysii4 '  or  a  '  habit  spasm,'  just  as  is  the  case  with  hysteri- 
cal aphonia  and  other  forms  of  habit  paralysis  which  can  be 
cured  by  re-education,  or  the  habit  spasms  which  we  often 
meet  with — of  which  some  cases  of  wryneck  and  writer's  cramp 
are  common  examples.  It  seems  quite  certain  that  the  sudden 
and  powerful  call  for  more  Ijlood  to  the  muscles  which 
resulted  from  the  game  of  tennis,  broke  down  the  habit  of 
sluggish  vaso-motor  response  to  the  ordinary  calls  for  blood 
which  walking  produced,  and  so  cured  his  intermittent 
claudication. 

I  have  met  other  cases  where  some  such  sluggishness  of 
the  vaso-dilator  mechanism  appeared  to  be  the  cause  of  the 
patient's  symptoms,  but  I  cannot  enter  upon  this  larger  subject 
within  the  scope  of  this  paper,  and  I  throw  out  this  suggestion 
in  the  hope  that  the  attention  of  others  may  l)e  directed  to  the 
possibility  of  such  a  condition. 

I  have  at  the  present  time  under  my  care  a  case  of  trouble- 
some neurasthenia,  where  the  symptoms  seem  explicable 
on  the  supposition  thai  the  arterial  l)lood  supply  is  not 
adequately  increased  by  vaso-dilatation  when  there  is  a  call 
for  increased  activity  of  the  brain. 

I  must  not  leave  this  subject  without  referring  to  a  class 
of  case  which  is  sometimes  difficult  to  differentiate  from  those 
cases  of  muscular  pain  from  malnutrition. 

I  refer  to  those  cases  where  the  muscles  are  painful  on 
exertion,  but  where  tenderness  on  pressure  apart  from  exertion 
is  an  extremely  marked  symptom. 

These  cases  were  first  brought  under  my  notice  by  a  little 
book  by  Dr.  Eabagliati  of  Bradford,  very  many  years  ago. 
In  them  the  muscular  tenderness  and  painfulness  suggests  some 
form  of  myositis  or  unusual  rheumatic  affection,  but  this 
theory  is  negatived,  I  think,  by  the  fact  that  the  condition  is 
curable,  as  Dr.  Rabagliati  pointed  out,  by  forcible  voluntary 
movements,  especially  if  combined  with  firm  pressure  over 
the  muscles — an  exercise  calculated  greatly  to  improve  their 
nutrition. 

It  may  ])e  that  here  too  we  are  dealing  with  a  vasomotor 
failure;  but  the  fact  that  the  muscles  are  in  some  cases  extremely 


DEFICIENT  BLOOD-SUPPLY  479 

tender  when  at  rest  seems  to  negative  the  possibility  that 
malnutrition  alone  is  the  cause.  It  is  of  interest  to"  note  that 
this  condition  of  extreme  muscular  tenderness  is  sometimes 
found  in  patients  suffering  from  muscular  hardening,  tenderness 
and  pain  in  the  colon  ;  and  it  is  far  from  improbable  that  the 
condition  is  really  due  to  the  appearance  in  the  voluntary 
muscles  of  a  condition  of  tonic  expansion  similar  to  that  which 
is  giving  rise  to  the  intestinal  symptoms  {vide  '  Pain  in 
Colitis,'  British  Medical  Journal,  June  1909). 

I  have  seen  several  cases  when  the  muscular  tenderness, 
curable  by  exercises,  involved  the  abdominal  muscles,  and  two 
where  it  involved  most  of  the  muscles  of  the  body,  but  especially 
those  of  the  abdomen  and  legs. 

As  regards  the  treatment  of  the  last  groups  of  cases  referred 
to,  the  important  indication  is  improvement  of  the  nerve  tone, 
and  massage  and  galvanism  with  full  feeding  are  valuable. 
It  is  also  very  important  to  look  out  for  and  combat  any 
possible  cause  of  neurasthenia  which  may  be  present.  Also 
it  must  not  be  forgotten  that  the  case  may  prove  one  of  the 
simple  ones  which  can  be  cured  by  violent  muscular  exercise, 
and  such  an  exercise  as  the  fashionable  one  of  skipping  is 
admirably  adapted  for  such  cases. 

I  feel  some  apology  is  needed  for  bringing  forward  these 
last-named  subjects  in  such  an  incomplete  form,  but  my 
doing  so  will,  I  hope,  lead  to  the  publication  of  other  cases 
which  may  give  fi-esh  light  as  to  the  cause  and  treatment 
of  these  as  j^et  somewhat  problematical  complaints. 


Essay  XVI.— ON  THE  VALUE  OF  EEVEEBERATION 
IN  THE  DIAGNOSIS,  AND  OF  GASTRIC  MASSAGE 
IN  THE  TREATMENT,  OF  ATONIC  STATES  OP 
THE  STOMACH  1 

Reverberation  in  Gastric  Diagnosis 

Although  we  have  many  means  at  our  disposal  for  the 
recognition  of  atonic  states  of  the  stomach,  any  addition  to 
our  diagnostic  armamentarium  will  doubtless  prove  acceptable. 
This,  therefore,  is  my  excuse  for  this  short  essay. 

I  have  for  some  time  used,  in  abdominal  diagnosis,  a  modi- 
fication of  the  old-fashioned  '  bell-sound  '  method  of  recognising 
large  cavities  in  the  lung,  or  the  presence  of  pneumo-thorax. 
As  commonly  used,  a  coin  pressed  on  the  skin  is  struck  by 
another  coin,  and  the  metallic  reverberation  of  the  sound  is 
audible  over  the  whole  of  the  cavity  under  examination.  In 
the  modification  referred  to,  instead  of  the  clinking  of  coins, 
reverberations  are  set  up  in  the  cavity  to  be  examined  hj 
scratching  with  the  finger-nail  a  roughened  rod,  which  is  firmly 
pressed  down  on  to  the  skin  overlying  it. 

When  listening  with  a  stethoscope  over  the  cavity  itself  the 
sound  has  a  distinctive  metallic  character,  and  when  the  stetho- 
scope is  not  over  the  cavity  the  scratching  sound  only  is  heard. 

The  area  over  which  the  scratching  sound  has  this  distinctive 
reverberating  character  defines,  with  great  accuracy,  the  area 
occupied  by  the  subjacent  air-containing  viscus,  and  the 
method  is  often  of  distinct  assistance  where  such  an  air- 
containing  organ  as  the  stomach  or  the  distended  colon  cannot 
be  accurately  mapped  out  by  ordinary  percussion.  It  is  of 
distinct  value  where  the  pitch  of  the  colon  or  intestinal  note 
happens  to  be  so  similar  to  that  of  the  stomach  note  ihat 

'  iSce  Binninghayn  Medical  Reinew,  1908. 
480 


REVERBERATION  IN  GASTRIC  DIAGNOSIS        481 

percussion  unaided  gives  an  uncertain  result.  Tliere  are  two 
ways  in  which  reverberation  can  be  practised,  and  sometimes 
one  and  sometimes  the  other  gives  the  best  results.  Supposing 
that  the  area  occupied  by  the  stomach  is  to  be  defined,  the 
roughened  rod  is  pressed  down  firmly  upon  some  spot  in  the 
epigastrium  where  tympanitic  gastric  resonance  is  well  marked, 
and  the  area  over  which  the  metallic  reverberation  is  audible 
is  carefully  noted  by  the  stethoscope.  The  alternative  pro- 
ceeding is  for  the  stethoscope  to  be  always  on  the  same  spot, 
over  the  stomach,  and  the  reverberator  moved  about.  When 
pressed  over  the  gastric  area,  metallic  reverberations  will 
be  heard  ;  when  not  over  it,  they  will  not  be  heard.  Of  the 
two  methods  the  former  is,  perhaps,  the  most  convenient,  if 
a  binaural  stethoscope  is  used,  as  it  can  be  more  easily  moved 
about  than  the  reverberator.  If,  however,  a  wooden  stetho- 
scope be  used,  the  second  method,  where  the  reverberator 
is  moved  about,  would  prove  the  most  convenient.  As  thus 
employed,  the  method  simply  shows  the  area  occupied  by 
the  stomach,  and  supplements  ordinary  percussion. 

It  can,  however,  be  made  to  give  useful  evidence  as  to  the 
amount  of  muscular  tone  present  in  the  stomach.  We  have 
but  few  direct  methods  of  ascertaining  this,  unless  the  stomach 
wall  be  contracted  enough  to  be  made  out  by  palpation  (as  is 
sometimes  the  case),  or  unless  there  be  sufficient  muscular  hyper- 
trophy for  the  waves  of  peristalsis  to  be  visible— as  in  pyloric 
stenosis,  &c.  If  both  the  stethoscope  and  the  reverberator 
be  over  the  stomach,  and  the  reverberator  be  continuously 
scratched,  and  with  an  unvarymg  degree  of  force,  the  pitch  of 
the  note  will  often  be  found  to  vary  from  to  time  time,  alter- 
nately rising  and  falling.  The  rise  in  the  pitch  of  the  note  is  due 
to  an  increase  in  the  tension  of  the  stomach  walls  and  of  the  gas 
within  it,  owing  to  muscular  contraction  or  other  cause,  and  a 
fall  in  the  note  being,  conversely,  due  to  lowering  of  the  tension 
by  muscular  relaxation.  Thus,  by  the  presence  or  absence 
of  this  change  in  the  pitch  of  the  note  it  is  possible  to  say 
whether  a  somewhat  enlarged  or  overfull  stomach  is  due  to  a 
spasmodic  contraction  of  the  pylorus  with  normal  or  even 
increased  tone  of  the  stomach  muscles,  or  whether,  on  the  other 
hand,  it  is  due,  not  to  hindrance  to  the  escape  of  the  gastric 

2  I 


482  Rp;VERBERATION  IN  GASTRIC  DIAGNOSIS 

contents,  but  to  a  defect  in  its  expulsive  power  owing  to 
muscular  atony.  In  a  flabby  atonic  stomach  there  would  be 
little,  if  any,  change  in  the  pitch  of  the  reverberation  note. 
With  a  little  experience,  it  is  sometimes  possible  to  say  at  once, 
on  hearing  the  reverberation  sound,  '  This  stomach  is  not 
atonic,  the  reverberation  note  has  a  high  pitch.' 

The  value  of  reverberation  in  gastric  diagnosis  was  evidenced 
by  a  case  recently  under  my  care  in  the  General  Hospital. 
The  patient  was  emaciated  and  there  was  something  suggestive 
of  Addison's  disease  about  her.  On  palpation  of  the  epigas- 
trium a  gurgling  was  occasionally  felt,  as  when  the  stomach 
empties  itself  through  a  slightly  narrowed  pylorus.  On  testing 
with  the  reverberator,  however,  although  the  gurgling  could  be 
distinctly  heard  during  the  examination,  the  pitch  of  the  gastric 
reverberation  note  remained  unchanged,  and  of  a  fairly  low 
tone.  This  showed  that  the  gurgling  was  not  of  gastric  origin. 
On  placing  the  reverberator  over  the  situation  of  the  transverse 
colon,  however,  and  Hstening  over  it,  it  was  found  that  there 
was  a  marked  change  in  the  pitch  of  the  note,  which  gradually 
ascended  till  the  gurgling  took  place,  and  then  dropped  again. 
On  further  investigation  it  was  found  that  on  placing  the 
reverberator  over  the  colon  to  the  left  of  the  middle  line,  and 
listening  near  the  hepatic  flexure  (or  vice  versa)  the  reverbera- 
tion note  could  occasionally  be  heard  from  the  ascending  to 
the  transverse  colon  and  occasionally  not,  and  that  the  period 
of  its  audibility  corresponded  to  the  periodicity  of  the  occm-- 
rence  of  the  gurgling ;  at  the  time  of  examination  about  once 
every  minute  or  two.  This  showed  conclusively  that  there 
were  peristaltic  weaves  in  the  transverse  colon — that  the  colon 
was  sometimes  unduly  distended,  allowing  the  reverberation 
note  to  be  audible  throughout  the  upper  part  of  the  ascending 
colon  and  the  whole  of  the  transverse  colon,  and  that  at  times 
this  continuitj^  in  its  lumen  was  broken  by  muscular  contraction 
in  the  region  of  the  hepatic  flexure. 

On  testing  the  descending  colon  it  was  found  that  the 
reverberation  note  was  never  obtainable  between  the  transverse 
and  the  descending  colon,  showing  that  there  was  some  inter- 
ference with  the  lumen  of  the  gut  in  the  neighbourhood  of  the 
splenic  flexure. 


REVERBERATION  IN  GASTRIC  DIAGNOSIS         483 

As  the  reverberation  note  seemed  to  be  always  obtainable 
throughout  the  transverse  colon,  the  latter  was  evidently  too 
dilated  to  be  obliterated  by  the  muscular  contractions,  and 
therefore,  the  stricture  in  the  region  of  the  splenic  tlexuro  could 
not  be  a  very  recent  one  or  a  very  slight  one.  The  presence  of 
a  partial  stiicture  of  the  colon  near  the  splenic  llexure  was  also 
suggested  by  the  fact  that  the  sigmoid  llexure  could  be  felt 
to  be  empty  and  of  norm?l  muscular  tone.  The  caecum  and 
ascending  colon  were  not  distinguishable  by  palpation. 

On  palpation  the  gurgling  could  sometimes  be  felt,  and  its 
situation  seemed  to  be  too  much  to  the  left  to  be  due  to  a  con- 
tracted pylorus ;  nevertheless,  wdthout  the  aid  of  reverberation 
the  diagnosis  could  not  have  been  cleared  up  as  it  was.  There 
was  no  tumour  to  be  felt,  and  nothing  abnormal  was  palpable  in 
the  left  hypochondrium  except  in  the  slight  gurgling  already 
mentioned,  which  occurred  every  minute  or  so.  The  stricture 
was  not  by  any  means  a  complete  one,  for  there  was  not  any 
serious  ditificulty  in  getting  the  bowels  open. 

Considering  the  cachectic  condition  of  the  woman  the 
recognition  of  this  interference  with  the  action  of  the  colon 
made  the  diagnosis  of  cancer  involving  or  originating  in  the 
splenic  flexure  of  the  colon  a  fairly  certain  one. 

I  have  recently  had  another  case  very  similar  to  the  one 
just  recorded,  but  in  neither  case  has  there  been  a  post-mortem 
examination  to  confirm  the  diagnosis. 

Although  such  cases  as  these  are  by  no  means  of  frequent 
occurrence,  they  suffice  to  prove  the  value  of  reverberation  as  a 
method  of  diagnosis,  and  in  ordinary  cases  of  gastric  derange- 
ment the  medical  practitioner  who  tries  it  will,  I  am  sure,  find 
it  a  useful  adjunct  to  other  methods.  It  does  not  need  any 
elaborate  apparatus.  For  many  years,  I  used  a  small  bone  rod 
some  one  and  a  half  inches  long,  with  a  roughened  top  which 
I  could  scratch  ;  but  of  late  years  I  have  used  a  much  simpler 
implement,  and  one  which  is  probably  in  the  hands  of  most 
medical  men  :  I  refer  to  the  small  five-shilling  stylographic 
pen.  When  closed,  it  is  under  four  inches  long  and  has  a 
roughened  ring  round  it  just  below  the  cap  to  facilitate  the 
unscrewing  of  the  writing-point.  If  the  pen  be  held  with  the 
lower  end  in  the  palm  of  the  hand  and  the  cap  pressed  against 


484  GASTRIC  MASSAGE 

the  wall  of  the  chest  or  abdomen,  this  roughened  ring  comes  at 
just  the  right  level  to  be  scratched  by  the  finger-nail  of  the  first 
or  second  finger. 

It  is  a  most  convenient  form  of  reverberator,  and  obviates 
the  necessity  of  adding  another  to  the  necessary  instruments  of 
precision  which  the  doctor  has  to  carry  with  him. 

Value  of  Massage  in  the  Treatment  of  Atonic  States  of 
THE  Stomach 

In  a  very  considerable  proportion  of  the  simpler  cases  of 
indigestion  which  we  have  to  treat,  an  atonic  state  of  the 
stomach  plays  an  important  part.  Catarrhal  conditions  of  the 
stomach,  and  lowered  vitahty  in  general,  are  extremely  apt  to 
lead  to  a  deficiency  in  the  hydrochloric  acid  of  the  gastric 
juice,  and  also  to  a  deficiency  in  the  muscular  power  of  the 
stomach;  These  two  conditions  both  bring  about  delay  in  the 
emptying  of  the  stomach,  and  cause  further  interference  with 
its  functions,  not  only  by  depriving  the  stomach  of  its  proper  rest 
between  meals  and  at  night,  but  also  because  the  remains  of  a 
preceding  meal  will  hamper  the  digestion  of  the  succeeding  one. 
The  usual  remedy  for  such  a  condition  is  the  familiar  acid 
and  nux  vomica,  with  or  without  pepsin,  after  meals  ;  but  a 
very  valuable  adjunct  to  this  treatment  is  a  form  of  massage 
calculated  to  assist  the  enfeebled  muscular  action  of  the 
stomach,  and  so  prevent  the  damage  done  to  the  mucous 
membrane  by  the  undue  retention  of  its  contents. 

Before  attempting  to  devise  a  means  of  helping  the 
muscular  action  of  the  stomach  by  massage,  we  must  study 
carefully  its  normal  muscular  movements.  This  can,  for- 
tunately, be  done  cHnically,  for  its  peristaltic  movements  are 
not  infrequently  visible  in  cases  where  there  is  some  pyloric 
obstruction  with  some  dilatation  of  the  stomach.  In  such  a 
case  the  passage  of  the  wave  of  peristalsis  is  sometimes  easily 
observable  and  its  characters  can  be  noticed. 

The  character  of  the  peristaltic  movements  of  the  stomach 
is  as  follows  : — 

1.  A  peristaltic  wave  consists  of  a  single  narrow  con- 
striction of  the  stomach,  which  commences  near  the  cardia 


GASTRIC  MASSAGE  485 

and  passes  down  towards  ilio  pylorus,  keeping  always  trans- 
verse to  the  diameter  of  the  stomach  ;  or,  to  express  it  other- 
wise, the  depression  due  to  the  contraction  is  along  the  line 
of  a  radius  of  the  circle  of  which  the  greater  curvature  is  the 
circumference. 

2.  Further,  the  waves  occur  singly  and  not  in  groups 
and  a  second  wave  does  not  begin  to  travel  down  across  the 
fundus  until  after  tlie  ])roceding  one  has  reached  the  pylorus. 

3.  As  to  rate:  The  rate  of  the  wave  is  not  quite  uniform. 
It  commences  rather  more  slowly,  and  quickens  slightly  as 
it  approaches  the  pylorus.  This  quickening  commences  to 
be  distinctly  appreciable  over  the  one-third  or  one-fourth 
of  the  stomach  at  its  pyloric  end.  The  wave  also  gains  in 
force,  and  is  more  distinctly  visible  over  the  pyloric  end  of  the 
stomach  than  over  the  fundus. 

Owing  to  the  distinctness  of  the  waves  it  is  quite  easy  to 
time  them.  In  an  active  stomach  it  will  be  found  that  they 
follow  each  other  at  intervals  of  about  twenty  seconds  over 
any  particular  part  of  the  stomach,  and,  as  they  follow  one 
another  without  any  interval,  their  periodicity  may  be  put 
down  as  about  three  per  minute.  In  a  less  active  stomach, 
half  a  minute  may  be  found  to  elapse  between  succeeding 
waves,  but  three  per  minute  may  be  taken  as  the  normal 
rate. 

This  periodic  contraction  may  also  be  estimated  by  the 
palpation  of  the  pylorus,  and  often  constitutes  a  valuable 
means  of  distinguisliing  the  pylorus  from  a  nodule  of  new 
grow^th,  or  an  enlarged  gland.  In  the  case  of  the  pylorus  its 
hardness  will  be  found  to  vary  periodically. 

The  knowledge  of  these  facts  makes  it  clear  that  move- 
ments of  the  hand  at  the  rate  usually  adopted  in  general  mas- 
sage will  not  be  calculated  to  aid  the  gastric  peristalsis,  but  will, 
on  the  other  hand,  be  apt,  in  the  feeble-acting  atonic  stomach, 
to  break  up  the  peristaltic  waves  and  hinder  rather  than  help 
the  stomach  in  its  efforts  to  empty  itself. 

In  gastric  massage,  effort  must  be  made  to  help  the  stomach 
in  two  directions.  Firstly,  the  endeavour  to  diminish  the  size 
of  the  enlarged  and  flabby  organ  so  as  to  give  the  weakened  and 
extended  muscles  more  purchase  in  their  effort  to  constrict  its 


480  riASTRIC  MASSAGE 

lumen  ;  and,  secondly.  l)v  means  of  slow  rliylhmically  varying 
pressure  to  simulate  the  action  of  the  peristaltic  waves,  and 
thus  accentuate  the  stomach's  own  efforts  to  force  its  contents 
through  the  pylorus. 

The  first  indication — that  of  diminishing  the  size  of  the 
stomach — can  be  met  by  endeavouring  to  support  the  lower 
border  of  the  stomach  by  the  hand  and  push  it  upwards.  To 
do  this  most  effectively  the  patient  must  lie  on  a  couch  with 
the  head  and  shoulders  slightly  raised,  and  with  the  abdominal 
muscles  relaxed.  Also,  for  gastric  massage,  the  patient  ought  to 
be  slightly  turned  towards  the  left  side  so  that  gravity  may 
draw  the  stomach  slightly  away  to  the  left  and  thus  luring  the 
axis  of  its  pyloric  end  into  line  with  the  axis  of  the  pylorus  and 
first  part  of  the  duodenum.  In  an  atonic  stomach,  such  as  we 
are  speaking  of,  if  the  patient  were  to  lie  on  the  left  side,  the 
stomach  would  be  apt  to  fall  away  rather  to  the  right  side,  and 
a  partial  kink  would  tend  to  be  produced  thereby  in  the  region 
of  the  pylorus. 

To  support  the  stomach  most  effectively  it  is  necessary  to 
use  the  right  hand  and  to  stand  on  the  right  side  of  the  patient, 
so  that  the  hollow  of  the  right  hand  may  coincide  with  the  curve 
of  the  lower  border  of  the  stomach,  and  also  so  that  general 
uniform  pressure  may  be  applied  over  the  stomach  in  the 
endeavour  to  keep  it  pressed  back  under  the  costal  arch  and 
towards  the  normal  position  of  the  pylorus.  The  ulnar  border 
of  the  hand  must  therefore  be  gently  placed  on  the  abdomen 
about  the  level  of  the  stomach's  lower  border  and  the  en- 
deavour made  to  gather  it  up  into  the  hollow  of  the  hand  by 
means  of  gentle  pressure  combined  with  a  lifting  and  shaking 
movement. 

When  this  is  done,  gentle  continuous  pressure  is  exerted 
by  the  hand  for  some  twenty  seconds  or  so,  and  then  the  pres- 
sure is  relaxed  and  the  hand  reapplied  as  before,  and  pressure 
continued  for  another  third  of  a  minute.  This  must  be  con- 
tinued for  ten  minutes  or  so.  This  simple  type  of  intermittent 
pressure  massage  is  decidedly  efi'ective  in  aiding  the  stomach  to 
empty  itself,  and  proof  of  this  may  be  found  in  the  fact  that 
after  applying  it  to  an  atonic  stomach,  which  still  contains  food, 
some  three  or  four  hours  after  a  meal,  it  will  be  found  to 


GASTKIC  MASSAGE  487 

empty  itself  very  considerably  if  not  entirely  in  the  course  of 
a  comparatively  few  minutes'  treatment. 

Sometimes  gurgling  due  to  the  passage  of  its  contents 
through  the  pylorus  will  be  felt  within  a  minute  or  two  of 
commencing  to  press  the  stomach. 

The  advantage  of  this  type  of  massage  is  that  it  can  be 
easily  learned  by  the  patient,  and  to  be  really  useful  this  is 
essential,  for  the  massage  ought  to  be  done  half  an  hour  or  so 
before  meal-times,  and  for  twenty  minutes  or  so  before  going 
to  bed  at  night,  so  as  to  lessen  the  risk  of  food  remaining  in  the 
stomach  all  night.  This  type  of  massage  is  extremely  beneficial 
to  the  patient,  although  of  less  direct  value  to  the  medical  prac- 
titioner, as  it  enables  the  patient  to  cm'e  himself  somewhat 
rapidly  after  he  has  once  been  taught  how  to  do  it. 

This  pressure  massage  is  rendered  more  efficacious  if,  while 
the  hand  is  being  pressed  over  the  gastric  area,  rhythmically 
varying  pressure  is  exerted  so  as  to  simulate  the  passage  of 
a  peristaltic  wave.  Thus,  to  commence  with,  the  finger-tips  are 
somewhat  more  firmly  pressed  into  the  abdomen  over  the 
fundus  of  the  stomach  than  the  rest  of  the  hand,  then,  after 
a  few  seconds,  pressure  is  made  specially  with  the  centres 
of  the  fingers  and  later  on  with  the  digital  border  of  the  palm. 
Then  the  hand  may  be  shifted  a  Httle  so  that  the  ball  of  the 
thumb  comes  to  be  over  the  situation  of  the  pylorus,  and  for 
the  last  eight  or  ten  seconds  pressure  is  specially  made  by  the 
ulnar  and  digital  border  of  the  palm,  so  as  to  press  the  gastric 
contents  towards  the  pylorus,  just  as  the  final,  more  powerful 
effort  of  the  normal  persistaltic  wave  does. 

After  twenty  seconds,  the  same  manipulation  is  practised 
again ;  the  stomach  is  afresh  gathered  up,  as  it  were,  into  the 
hollow  of  the  hand  and  pressure  begun  by  the  finger-tips  just 
under  the  costal  arch  over  the  fundus,  and  then  slowly  the 
stomach  is  pressed  on  nearer  and  nearer  to  the  pylorus,  until 
during  the  last  one-third  or  one-fourth  of  the  twenty-seconds' 
period  the  pyloric  end  of  the  stomach  mainly  is  pressed  on  and 
in  a  direction  towards  the  pyloric  orifice. 

As  will  be  gathered  from  this  description,  the  hand  must  be 
flexible  and  well  trained  in  order  to  exert  a  varying  pressure  by 
first  one  and  then  another  part  of  it  without  relieving  altogether 


488  GASTRIC  MASSAGE 

the  pressure  of  the  rest  of  the  hand.  It  would  be  of  httle  value 
for  the  pyloric  end  of  an  atonic  stomach  only  to  be  pressed  on, 
for  the  contents  would  simply  be  pressed  into  the  fundus.  If 
however,  general  pressure  can  be  exerted  over  the  whole  of  the 
stomach  with,  at  the  same  time,  extra  pressure  localised  over 
the  pyloric  end,  the  effect  is  very  considerable.  When  skilfully 
applied  this  varying  pressure  massage  is,  in  my  experience,  a 
potent  means  of  emptying  an  atonic  stomach.  In  the  case  of  an 
educated  patient  this  type' of  massage  can  also  sometimes  be 
taught,  but  the  '  horny  hand  '  of  the  son  or  daughter  of  toil 
is  incapable  of  the  differential  movements  necessary  to  produce 
a  regularly  varying  degree  of  pressure  on  one  part  of  the 
stomach  during  the  maintenance  of  a  general  pressure  over 
the  whole  organ.  In  cases,  however,  where  the  patient  has 
been  able  to  learn  this  more  complicated  form  of  pressure 
massage,  I  have  often  been  astonished  at  the  rapidity  of  the 
improvement  in  the  gastric  tone,  and  the  patient  has  been 
most  pleased  at  the  result,  and  especially  at  the  increase  in  his 
comfort  at  night,  due  to  his  being  able  to  get  the  stomach  to 
empty  itself  prior  to  his  going  to  sleep. 

It  is  the  efficacy  of  this  form  of  massage  which  induces  me 
to  dwell  at  such  length  upon  this  subject. 


Essay  XVIL— A  CASE  OF  AEHYTHMIA  WHICH 
THEOWS  NEW  LIGHT  UPON  THE  VENOUS  PULSE 
AND  THE  ACTION  OF  THE  AUEICLESi 

A  FEW  words  must  be  said  hy  way  of  introduction  to  this 
essay. 

In  the  fu'st  place  the  writer  does  not  expect  that  this  essay 
wdll  prove  of  interest  to  any  but  those  who  are  maldng  a  special 
study  of  the  heart  by  means  of  graphic  records,  and,  moreover, 
to  many  of  them  his  interpretations  will  be  so  contrary  to  the 
usually  accepted  ones  that  few  will  probably  care  to  make 
the  mental  exertion  of  trying  to  follow  them. 

Nevertheless,  this  essay  forms  an  important  part  of  the 
message  which  the  writer  desires  to  make  public. 

Also  this  essay  may  be  criticised  upon  the  ground  that  the 
tracings  are  not  sufficiently  important  to  l)e  worth  so  much 
stud3^  In  answer  to  this  the  writer  w^ould  say  that  he  has 
given  this  series  of  tracings  as  typical,  and  that  the  methods 
of  interpretation  here  given  are  applicable  to  other  types  of 
tracing. 

Fault  ma}^  also  be  found  with  these  tracings  upon  the 
ground  that  the  cardiograms  here  given  are  different  from  those 
usually  obtained  by  the  Mackenzie  potygraph,  and  their 
accuracy  may  on  that  account  be  thought  to  be  open  to  doubt. 

The  answer  to  this  criticism  is  that  they  are  different,  because 
they  are  taken  hj  a  different  apparatus  from  that  usually 
supplied  with  the  [Mackenzie  polygraph.  Whatever  may  be  the 
advantages  of  the  cup  for  the  record  of  the  cardiac  move- 
ment it  has  the  disadvantage  that  it  gives  only  a  generalisation 
as  to  the  movements  of  the  heart. 

In  the  apparatus  used  hj  the  writer,  the  principle  of  Marey's 

1  Subject  of  a  communication  prepared  for  the  Dublin  meeting  of  the 
Association  of  Physicians,  1909. 

489 


490  A  CASE  OF  ARHYTHMIA 

sphygmograph  and  Gala  bin's  excellent  cardiograph  have  been 
adapted  to  the  Mackenzie  polygraph.  In  this  way  the  move- 
ment of  a  very  small  area  of  the  heart,  as  transmitted  through 
the  chest  wall,  is  recorded  and  magnified  by  mechanical  means 
before  being  conducted  by  air  to  the  waiting  tambours. 

In  the  opinion  of  the  writer,  the  true  relationship  between 
cardiac  activity  and  the  venous  pulse  can  only  be  adequately 
studied  by  some  such  apparatus. 

This  essay  may  also  be  thought  to  be  needlessly  full  of 
detail.  But  as  is  pointed  out  in  its  com'se,  an  explanation  of 
a  cardiogram  cannot  be  accepted  as  accurate  unless  it  suffices 
to  explain  adequately  the  main  features  of  the  tracing. 

In  the  present  instance  there  are  sometimes  as  many  as 
sixteen  or  eighteen  distinct  waves  associated  with  each  cardiac 
cj'^cle,  and  the  adequate  explanation  of  these  cannot  be  expected 
to  be  very  brief — more  especially  as  the  explanation  can,  in 
many  cases,  only  be  arrived  at  by  comparison  with  other  tracings 
which  in  their  turn  need  to  be  explained. 

The  explanation  of  the  tracings  here  given  is,  in  some 
instances,  only  tentative  ;  but  the  writer  feels  confident  that 
the  tracings  will  be  adequate  to  convince  anyone  who  has  the 
patience  to  think  them  out  along  the  lines  suggested  in  this 
essay. 

In  order  that  the  accuracy  of  the  correlation  of  the  various 
tracings  with  one  another  may  be  tested,  the  commencement 
or  ending  of  the  tracing  is  always  given  when  possible.  When 
this  is  not  done,  as  in  the  case  of  some  of  the  photographic  en- 
largements, the  original  tracing  from  which  the  enlargement 
was  made  is  given  in  order  that  the  corresponding  points  in 
the  venous  and  ventricular  portions  may  be  measured  by  any 
reader. 

Summary  of  the  Argument  ^ 

Careful  study  of  the  graphic  records  of  the  case  here  de- 
scribed seems  clearly  to  prove  the  following  propositions  : — 

1.  The  ventricles  of  the  heart  fill  themselves  by  their  own 
expansion. 

2.  So    far  as    sensitiveness    to  mechanical  stimulation    is 

'  For  summary  of  facts  and  theories  here  brouglit  forward,  see  p.  r)23. 


WITH  EXTRA  SYSTOLES  491 

concerned  (here  is  for  the  ventricles  no  non-excitable  '  latent 
period.' 

3.  The  ventricles  can  be  stimulated  to  contract  immediately 
after  the  normal  systole,  by  over-distension — the  result  of  their 
own  expansile  act — thus  causing  an  extra  systole. 

4.  There  is  for  the  auricles  no  '  latent  '  or  non-excitable 
period,  so  far  at  all  events  as  mechanical  stimulation  by  dis- 
tension is  concerned.  A  definite  contraction  can  be  caused 
shortly  after  the  auricular  systole  by  the  inrush  of  1)lood 
regurgitating  from  the  ventricle. 

5.  There  is  no  true  relaxation  or  passivity  of  the  muscular 
walls  of  the  auricle.  They  remain  in  a  state  of  tonic  activity 
throughout  the  diastole. 

6.  The  walls  of  the  auricle  are,  throughout  the  diastole, 
SENSITIVE  to  any  sudden  changes  of  pressm-e  within  it,  and 
respond  by  increase  of  tonic  activity  or  by  contraction,  to  any 
force  tending  to  distend  it,  or  to  any  reHef  of  pressure  within  it. 

7.  The  GREAT  VEINS,  by  means  of  their  tome  activity, 
maintain  the  blood  pressm-e  within  them  at  the  same  level 
as  that  within  the  auricle  and  ventricle  (during  their  relaxation 
phase),  and  at  such  a  height  that  the  blood  in  the  right  side 
of  the  heart  and  veins  acts  as  one  continuous  column  of  liquid 
within  firm  walls,  the  conduction  of  impulses  being  thus 
rendered  practically  instantaneous. 

8.  The  walls  of  the  great  veins  are  sensitive  to  sudden 
variations  in  the  pressure  withm  them,  and  respond  by  in- 
creased tone  or  by  a  definite  act  of  contraction  to  stimulation 
by  sudden  distension.  Such  contraction  may  be  observable 
in  venous  tracings  if  the  distensible  force  be  not  great  enough 
to  overpower  the  muscles  of  the  veins,  or  so  prolonged  that 
the  stimulus  to  contract  loses  its  effect  before  the  pressure 
is  sufficiently  relaxed  to  admit  of  the  contraction  emptying 
the  vein.  The  vein  may  also  be  stimulated  to  contract  by  a 
sudden  decrease  in  the  intravenous  pressure. 

Introductory 

During  recent  years  a  great  stimulus  has  been  given  to 
the  study  of  the  heart  by  means  of  graphic  methods,  not  only 


492  A  CASE  OF  ARHYTHMIA 

by  the  writings  of  Hir  J.  Mackenziu,  and  others,  but  also  far 
more  by  the  extremely  practical  and  convenient  polygraph 
which  we  owe  to  him. 

The  clinical  work  has,  however,  been  largely  along  one 
line — namely,  the  study  of  disorders  in  the  conductivity  of 
stinnili  through  the  heart  muscle,  and  man}'^  records  are  being 
published  of  venous  tracings  which  show,  or  seem  to  show, 
auricular  contractions  which  are  not  transmitted  to  the  ven- 
tricles and  which  are  apt  to  be  taken  as  evidence  of  a  greater 
or  less  degree  of  heart-block  in  the  patients  concerned. 

One  object  of  this  paper  is  to  draw  attention  to  a  case 
which  seems  to  show  clearly  that  the  auricles  and  ventricles 
are  both  sensitive  to  mechanical  stimulation  and  that  extra- 
systoles  may  be  explicable  in  this  way  quite  apart  from  faults 
in  conductivity. 

Now  the  interpretation  of  graphic  records  of  the  heart 
or  veins  is  by  no  means  as  simple  as  it  appears  ;  and  I  have 
not  infrequently  seen,  in  the  medical  journals,  venous  tracings 
interpreted  in  a  manner  which  may  have  been  accurate,  but 
of  whose  accuracy  the  tracings  given  afforded  no  proof.  The 
importance  of  a  mistake  in  interpretation  may  be  very  great, 
because  the  presence  of  extra  systoles  of  the  auricle  is  apt 
to  be  taken  as  a  sign  of  some  serious  defect  in  the  conductivity 
of  impulses  through  the  heart,  and  suggests  a  bad  prognosis. 

Now  waves  in  the  neck  veins  may  occur  which  closely 
resemble  auricular  pulsations,  but  which  are  not  of  auricular 
origin,  and  there  may  be  extra  systoles  of  the  auricle,  as  this 
case  seems  to  show,  which  are  the  result  of  mechanical  stimula- 
tion and  whose  occurrence  does  not  indicate  any  abnormality 
of  conductivity. 

Therefore,  it  is  necessary  to  compare  the  venous  tracing 
with  a  carefully  taken  apical  one  before  a  reliable  interpretation 
of  it  can  be  made  and  before  it  can  be  asserted  that  the  auricles 
are  acting  independently  of  the  ventricles,  or  that  anything 
of  the  nature  of  delayed  conductivity  is  present.  *  But,  unfor- 
tunately, interpretation  of  a  cardiogram,  as  is  the  case  with 
other  clinical  problems,  closely  resembles  the  interpretation 
of  a  sentence  of  a  foreign  language  :  you  cannot  be  certain 
of  its  meaning  till  you  know  the  meaning  of  every  word.     A 


WITH  EXTRA  SYSTOLES  493 

word  left  untranslated  may  be  the  '  not  '  or  (he  '  never  ' 
which  enth'ely  reverses  the  whole  meamng  of  the  sentence. 
An  illustration  of  this  is  given  at  p.  519. 

Therefore,  before  I  can  use  my  tracing  as  evidence,  I  must 
show  that  my  interpretation  holds  good  for  every  wa^  e  and 
oscillation  in  it,  and  as  there  are  sometimes  sixteen  distinct 
waves  for  one  beat  of  the  heart  the  task  of  interpretation  must 
put  some  strain  upon  the  patience  of  the  reader. 

But  before  going  into  the  cardiographic  evidence,  I  must 
describe  the  case  in  its  main  bearings. 

The  patient  was  a  .young  man  aged  twenty-one  years,  a 
gardener  by  occupation.  There  had  been  a  gradual  onset  of 
shortness  of  breath  for  the  last  year  or  so,  combined  with  some 
pain  in  the  left  shoulder  when  working  with  the  left  hand. 
For  the  last  one  or  two  months  he  had  had  occasional  attacks  of 
faintness  and  sudden  feeling  of  weakness,  causing  him  to  stop 
work  and  sit  down  if  they  came  on  by  day.  More  usually,  how^- 
ever,  the  attacks  came  on  at  night,  would  sometimes  last  an  hour, 
and  were  sometimes  accompanied  by  vertigo — a  sense  of  objects 
turning  round  him  ;  also  he  occasionally  had  stabbing  pain  in 
the  left  side  of  the  chest  on  exertion — such  as  lifting  a  heavy 
weight.  He  has  not  been  able  to  work  for  three  months.  He 
had  leg  pains  on  exertion — e.g.  after  walking  a  mile  or  so  a 
sensation  of  weakness  in  his  legs  would  come  on,  accompanied 
by  aching  pain  in  the  calves,  which  lasted  for  an  hour  or  so 
after  ceasing  to  work.  His  feet  were  always  cold,  and,  though 
walking  would  warm  them  for  a  time,  they  would  go  cold  again, 
especially  when  the  pain  came  on. 

There  was  evidence  of  weak  cardiac  action  in  the  fact 
that  the  gastric  resonance  was  an  interspace  too  high,  that 
the  liver  dullness  was  small,  the  dullness  of  its  left  lobe  being 
absent,  and  that  of  its  right  lobe  not  reaching  to  the  costal 
arch.  Although  the  man  was  well  nourished  and  healthy 
looking,  it  was  quite  evident  from  his  symptoms  and  the 
condition  of  his  liver  and  diaphragm  that  the  heart  was  not 
able  to  keep  the  proper  amount  of  blood  in  circulation. 

On  listening  to  the  heart  there  was  no  murmur,  but  con- 
siderable irregularity,  consisting  in  coupled  beats — namely,  a 
normal  one  closely  followed  by  a  short  imperfect  one.  which  the 


494 


A  CASK  OF  ARIIYTHMIA 


ciirdiogiiiph  showed  to  be  an  extra  ventricular  systole.     Al- 
though the  extra  systole  alternated — as  a  rule  with  the  normal 


Fig.  l.JO. — Tracings  from  the  Apex  and  the  Carotid  Artery, 
SHOWING  that  the  Extra  Systole  causes  no  Pttlsb  Wave  in  the 
Artery  and  that  the  Wave  following  an  Extra  Systole  is  smaller 
than  normal. 

This  is  copied  from  fitr.  1,  Plate  IX,  and  is  uot  drawTi  to  scale.) 

beat — it  occasionally  occurred  less  frequently,   i.e.  once    in 
three  or  four  beats. 


Fig.  157. — Copy  of  a  Tracing  showing  a  Wave  in  the  Jugular  Vein 
which  results  from  the  Extra  Systole. 

On  taking   simultaneous  tracings  of   the  apex  beat  and 
of  the  carotid  artery  and  of  the  apex  and  external  jugular 


WITH  EXTRA  SYSTOLES 


4'.)5 


vein  tho  reason  iov  tlio  cardiac  inojfiicioiicy  was  apparent, 
for  tho  extra  s^ystole  did  not  as  a  rule  succeed  in  forcing  Ijlood 
into  the  aorta,  there  being  no  carotid  pulse  wave  corresponding 
to  it,  whereas  there  was  a  distinct  wave  in  the  veins  of  the 
neck.  Moreover,  when  the  extra  systole  occurred  less  often 
than  with  alternate  beats,  it  was  evident  that  the  carotid 
pulse  wave  succeeding  the  extra  systolic  was  smaller  and  less 
eli'ective  than  that  duo  to  the  other  ventricular  contractions 
{vide  figs.  156  and  157). 

The  extra  systole,  therefore,  not  only  weakened  the  heart 
in  so  far  as  it  was  a  useless  contraction,  but  also  it  interfered 
with  the  amount  of  blood  sent  forward  by  the  succeeding 
normal  beat. 


Cause  of  the  Extra  Systole 

The  extra  systole,  as  has  been  said,  occurred  immediately 
after  the  preceding  normal  contraction.     On  studying  (in  the 

A/^^e  recora/ 
^'^■T  second 


Apex 

Ccbra/iogTAm 


/Record  of 
h(/  e/ectr/c  s/^ndJ 


Fiu.    158.- 


^■0      <^ 
-Copy  of 


Tracing  upon  which  the  Time  of  Occurrence  of 


THE  First  and  Second  Sounds  was  marked  by  an  Electric  Signal. 

It  shows  that  tlie  closure  of  the  semilunar  valves  takes  place  about  one-tenth  of  a  second 
before  the  end  of  the  systolic  rise  in  the  tracing.  Its  time  of  occurrence  is  marked  by  a  wave 
in  this  tracing.    (Not  drawn  to  scale.) 

cardiogram)  its  relationship  to  the  preceding  beat,  it  is  seen 
that  it  occurs  immediately  after  the  return  of  the  systolic  rise 
to  the  normal  level.  This  point  in  the  cardiogram  marks  the 
commencement  of  the  phase  of  ventricular  relaxation  and  the 
termination  of  the  short  period  (one-tenth  second  or  so)  of 
active  expansion,  during  which  the  ventricle  expands  with 
hardened  wall  and  fills  itself  by  its  own  aspiration.  In  the 
accompanying  cardiogram  the  position  of  the  second  sound  has 
been  marked  by  an  electric  signal  {vide  fig.  158).     Its  position 


496  A  CASE  OF  ARHYTHMIA 

is  sufficiently  accurate  to  show  that  the  last  wave,  before  the 
fall  of  the  lever  to  normal,  marks  the  point  when  the  semi- 
lunar valves  close.  This  point,  as  measured,  is  about  one- 
tenth  of  a  second  before  the  tinal  fall  of  the  lever.  Thus  the 
cardiogram  proves  that  the  extra  systole  occurs  exactly  at  the 
end  of  the  expansion  period — namely,  when  the  ventricle  has 
filled  itself  by  its  own  expansion. 

This  relationship  of  the  extra  systole  to  the  normal  systole 
appears  to  be  quite  constant  in  the  tracings,  and  so  far  as  simple 
inspection  can  tell  there  seems  to  be  no  variation  in  its  position. 
The  same  is  true  of  careful  measurements. 

Measured  Position  of  the  Extra  Systole. — On  measur- 
ing the  exact  position  of  the  extra  systole  in  relation  to  the 
preceding  ventricular  contraction,  it  is  found  that  its  relation- 
ship to  that  event  is  constant,  thus  confirming  the  cardiographic 
observation  as  to  its  occurrence  immediately  after  the  cessation 
of  the  cardiac  activity  due  to  the  preceding  beat.  Its  situation 
was  measured  on  the  cardiogram  in  eighty  instances,  and  the 
average  time  elapsing  between  the  start  of  the  extra  systole 
and  that  of  the  preceding  beat  was  0-446  of  a  second — a  usual 
length  of  time  for  this  part  of  the  cardiac  cycle.  The  range  of 
variation  in  any  one  series  of  observations  was  very  small. 
For  instance,  thirty  extra  systoles  gave  an  average  of  0-45 
second ;  but  out  of  these  in  only  three  instances  was  the 
time  of  occurrence  0-03  second  less  than  the  average,  and  in 
only  four  beats  was  it  as  much  as  0-03  second  more  than 
the  average. 

When  the  mode  of  action  of  the  heart  was  altered  by  drugs 
some  variation  was  noticeable. 

Thus  when  taking  strophanthus,  the  extra  systole  occurred 
on  the  average  0-386  of  a  second  after  the  commencement  of 
the  preceding  systole. 

When  under  the  influence  of  digitalis,  the  average  was 
0-47  of  a  second.  When  taking  aconite,  there  was  a  greater 
variation,  and  occasionally  the  depressing  effect  of  the  aconite 
showed  itself  by  a  lengthening  of  the  interval  between  the 
commencement  of  the  normal  systole  and  of  the  extra  systole, 
in  addition  to  the  lessening  of  the  frequence  of  the  extra  systoles. 
Thus  seven  extra  systoles  out  of  fourteen  in  one  tracing  gave 


WITH  EXTRA  SYSTOLES  497 

an  interval  of  0*5  second  and  two  of  them  of  only  0*42  second. 
The  average  of  the  fourteen  extra  systoles  being  0*476  second. 

Nevertheless,  these  variations  do  not  conflict  with  the 
statement  already  made — namely,  that  the  extra  systole  always 
occurs  at  the  point  where  the  cardiac  activity  ceases. 

This  point  marks  the  end  of  the  expansion  phase,  and  on 
the  cardiogram  it  is  the  lowest  point  reached  of  the  tracing 
after  the  systolic  rise. 

It  may,  therefore,  be  said  definitely  that  in  this  case  the 
extra  systole  occurred  exactly  at  the  end  of  the  expansion 
phase  of  the  cardiac  cycle.  In  other  words,  the  adventitious 
contraction  does  occur  just  when  the  ventricle  has  finished 
drawing  blood  into  itself  by  its  own  active  expansion. 

Proof  that  the  Ventricles  do  Fill  Themselves  by 
Their  own  Expansion. — This  case  affords  evidence  that  the 
major  part  of  the  filling  of  the  venticles  does,  as  already  affirmed, 
occur  during  the  expansion  phase  of  the  cardiac  cycle,  as  was 
advocated  twenty  years  ago  by  Dr.  Mayo  Collier.  The  fact  that 
an  effective  contraction  can  take  place  one-tenth  of  a  second  after 
the  ventricle  has  emptied  itself  must  be  taken  as  evidence,  that, 
during  that  one-tenth  of  a  second,  the  ventricle  has  been  refilled. 
That  the  contracti(m  is  effective  is  proved  by  its  power  of  pro- 
ducing so  distinct  a  wave  in  the  veins  of  the  neck  {vide  fig.  157). 
That  the  filling  is  done  by  ventricular  aspiration  is  proved  by 
the  absence  of  any  auricular  contraction  whereby  the  ventricle 
could  be  filled,  as  is  shown  by  the  tracings  {vide  fig.  159). 

The  extra  systole  is  due  to  over-distension  of  the 
ventricles. 

The  occurrence  of  the  extra  systole  at  the  precise  point  when 
the  ventricle  has  filled  itself  is  strongly  suggestive  of  the 
probability  that  a  stretching  of  its  muscular  walls  by  over- 
distension is  the  cause  of  the  extra  systole.  If  this  overfilling 
did  occur  and  the  ventricle  could  be  stimulated  to  contract 
by  the  overstretching  of  its  wall,  the  contraction  would  take 
place  precisely  at  the  time  when  the  extra  systole  does  occur 
in  this  case.  If  this  were  so,  there  would  be  three  factors  at 
work : — 

1.  Undue  irritability  of  the  heart. 

2.  Excessive  aspiratory  force. 


198 


A  CASE  OF  ARHYTHMIA 


3.  Abnormal  supply  of  blood,  from  am-icular  dilatation 
or  other  cause. 

The  effect  of  variation  in  these  factors  can  be  studied. 
Variation  in  the  first  factor  will  not  give  evidence  either  for 
or  against  this  theory.  Variation  in  the  second  factor  will 
give,  however,  important   evidence  if  it  can   be  shown  that 


Apex 


Vein 


Fig.  159. 


This  tracing  (wbicli  is  a  copy  of  a  portion  of  that  s1iov\ti  in  Tlate  XI,  Xo.  7)  demonstrates 
tlie  fact  tliat  there  is  no  sign  of  any  auricular  wave  preceding  the  extra  systole,  and  that  therefore 
the  fuUness  of  the  ventricle  with  blood  (which  the  occurrence  of  the  extra  systole  shows)  must  bo 
due  to  the  ventricle  having  filled  itself  by  its  own  expansion.  See  also  fig.  157  for  absence  of 
auricular  waves  in  the  vein  prior  to  the  extra-ventricular  systole. 


increase  of  the  aspiratory  force  of  the  ventricle  increases 
the  cardiac  irregularity  and  that  diminution  of  that  force 
diminishes  that  irregularity. 

Now,  digitalis  has  the  power  of  increasing  the  aspirator}^ 
force  of  the  cardiac  muscle,  and  aconite,  by  making  the  mus- 
cular contraction  more  sluggish,  will  lessen  both  the  elastic 
and  the  muscular  recoil  of  the  heart  wall  after  its  contraction. 
Digitalis,  therefore,  ought  to  increase  and  aconite  ought  to 
lessen  the  irregularity  of  the  heart  if  the  theory  here  advanced 
be   correct.     This   was   found   to   be   the   case.     Tincture   of 


WITH  EXTRA  SYSTOLES  499 

digitalis  in  twenty-minim  doses  every  four  hom'S  was  given,' 
with  the  result  that  the  irregularity  was  greatly  increased. 
Unfortunately,  some  of  the  tracmgs  taken  while  the  patient 
was  on  digitalis  have  been  lost,  and  the  "dates  were  omitted 
from  others.  Tracing  No.  8,  Plate  XI,  does,  however,  I 
believe,  show  the  effect  of  digitalis  and  the  marked  increase 
of  irregularity  caused  by  it.  Tracing  No.  7,  Plate  XI,  shows 
a  similar  tj^pe  of  irregularity,  and  it  was  certainly  taken 
during  the  adminstration  of  digitalis. 

In  contrast  with  this,  tincture  of  aconite  in  two-minim 
doses  every  two  hours  was  given,  with  the  result  that  the 
irregularity  was  very  greatly  lessened.  The  action  of  the 
aconite  in  making  the  beat  more  sluggish  may  be  seen  in  the 
lengthening  of  the  systole  from  an  average  of  0-45  second 
before  the  drug  was  given  to  an  average  of  0*47  second  while 
under  its  influence,  and  for  some  beats  to  as  much  as  0*5  of  a 
second.  Under  aconite,  the  frequency  of  the  extra  systoles 
dropped  from  one  in  two  beats  to  about  one  in  five  beats 
(e.g.,  forty-seven  in  ninety-seven  beats  and  seven  in  thu'ty-six 
beats).  Later  on  tinct.  digitalis  (nixx)  every  six  hours  was 
tried  again,  but  again  it  produced  a  sort  of  double  extra 
systole  every  fourth  beat  or  less.  After  this,  strophanthus 
was  given — -which,  in  my  opinion,  has  much  less  power  of  in- 
creasing the  ventricular  expansion  than  digitalis  has  (and  is 
therefore  of  more  value  in  aortic  regurgitation  than  digitalis 
is) — ^with  the  result  that  the  heart  again  became  more  regular 
and  the  extra  systole  dropped  in  frequency  to  once  in  nine  beats 
(eight  in  seventy-two  beats),  though  occasionally  it  occurred  as 
often  as  once  m  four  beats  (eleven  in  fifty).  The  patient  also 
felt  much  better  on  this  drug,  and  gradually  improved  and  was 
discharged.  Variation,  therefore,  in  the  second  factor  strongly 
confirms  the  theory  that  the  extra  systole  is  due  to  mechanical 
stimulation  resulting  from  over-distension  of  the  ventricle  by 
its  own  aspirating  force. 

Confirmatory  evidence  may  also  be  obtained  from  variations 
in  the  thhd  factor — namely,  in  the  amount  of  blood  supplied 
to  the  ventricle. 

Now  the  amount  of  blood  supplied  to  the  right  ventricle 
is  apt  to  vary,  in  consequence  of  the  resph-atory  movements 

■2  K  2 


500  A  CASE  OF  AEHYTHMIA 

of  the  chest.  Insph'ation  naturally  tends  to  draw  blood  mto 
the  thoracic  veins,  and,  the  return  of  this  blood  being  prevented 
by  the  valves  at  the  root  of  the  neck,  the  commencement  of 
expiration  naturally  tends  to  increase  the  pressure  upon  the 
blood  thus  enclosed,  and  so  favour  its  entry  into  the  right 
ventricle.  This  will  mainly  affect  the  first  beat  which  occurs 
after  the  end  of  expiration. 

This  is  of  course  the  secret  of  the  well-known  rehef 
given  by  '  the  long  breath  '  in  anaemic  dilatation  of  the  right 
ventricle. 

Moreover,  careful  measurement  of  the  loudness  of  the  right 
ventricular  sounds  demonstrates  the  same  fact ;  for  the  pulmo- 
nary second  sound  and  the  right  ventricular  murmurs  are  often 
measurably  louder  in  the  case  of  the  first  cardiac  beat  that 
occurs  during  expiration  than  in  the  rest  of  the  cycle.  These 
facts  show  that  the  first  beat  to  occur  after  the  end  of  in- 
spiration is  apt  to  be  more  effective  than  others,  owing  to  the 
ventricle  being  then  at  its  fullest.  Now  in  this  patient  it  was 
sometimes  noticed  that  the  extra  systole  only  occurred  at 
the  end  of  inspiration — namely,  as  has  been  shown,  when  the 
right  side  of  the  heart  was  extra  full  of  blood  and  there  was 
the  likelihood  of  an  excess  of  blood  being  aspirated  into  the 
ventricle  {vide  Tracing  No.  3,  Plate  IX).  Therefore,  variation 
of  the  third  factor  also  supports  this  theory. 

Action  of  the  x\uricles  and  Great  Veins 

This  case  also  throws  light  upon  the  activities  of  the  auricle 
and  great  veins.  My  study  of  venous  tracings  in  this  and  other 
cases  has  convinced  me  that — in  abnormally  worldng  hearts, 
at  all  events,  if  not  in  all  human  hearts — the  auricle  does  more 
work  than  it  appears  to  do  when  investigated  in  the  physio- 
logical laboratory.  Tracings  taken  in  one  instance  from 
over  the  auricle  itself  also  confirmed  this  view,  for  where 
there  is  tricuspid  regurgitation  the  auricle  appears  sometimes 
to  remain  contracted  throughout  the  greater  part  of  the 
ventricular  systole  {vide  Plate  XII,  No.  9). 

This  case  will,  I  think,  show  quite  clearly  to  those  who  make 
the  necessarv  effort  to  think  out  the  tracings,  that  the  auricle 


WITH  EXTRA  SYSTOLES  501 

is  ill  a  state  of  tonic  activity  throughout  the  cardiac  cycle,  and 
is  prepared  to  respond  by  increased  tonic  activity,  or  by  actual 
contraction,  to  any  sudden  increase  of  pressure  tending  to 
distend  it. 

But,  to  demonstrate  this  fact,  the  blood  which  regurgitates 
from  the  right  ventricle,  during  the  extra  systole,  must  be  very 
carefully  followed. 

Work  Done  by  the  Extra  Systole 

The  extra  systole,  as  already  pointed  out,  does  not,  as  a 
rule,  succeed  in  forcing  blood  into  the  aorta,  for  it  causes  no 
wave  in  the  carotid  artery.  Therefore,  presumably,  its  energy 
is  expended  in  forcing  blood  back  into  the  auricles  and  veins. 

Before  going  further,  it  were  well  to  point  out  that,  in  obtain- 
ing cardiographic  evidence  as  to  what  is  taking  place  in  the 
heart  and  veins,  it  is  sometimes  necessary  to  turn  to  the  right 
side  of  the  heart  and  sometimes  to  the  left  side,  upon  the  hypo- 
thesis— which  must  be  accepted — that  the  two  sides  of  the  heart 
act  in  unison.  All  the  evidence  here  points  to  the  fact  that 
the}^  do  so  act. 

Wave  in  Veins  Due  to  the  Extra  Systole. — In  the 
jugular  bulb,  there  is  a  well-marked  wave,  which  I  have  spoken 
of  as  being  due  to  tricuspid  regurgitation,  the  result  of  the 
extra  systole.  Careful  measurements  prove  that  this  is  its 
true  explanation,  although,  at  first  sight,  it  might  be  easily 
mistaken  for  a  wave  due  to  an  auricular  systole  :  so  much  so, 
that  an  eminent  authority  on  venous  tracings, to  whom  I  showed 
this  one,  expressed  his  belief,  after  superficial  examination, 
that  it  was  probabl}'  an  auricular  wave.  Therefore,  the  proof 
of  its  ventricular  origin  must  be  gone  into  somewhat  in  detail, 
although  it  involves  a  close  study  of  the  tracings. 

Eecoil  Waves  in  the  Apex  Cardiogram. — If  the  extra 
systole  be  examined  it  will  be  seen  that  the  rise  it  causes  in  the 
cardiogram  is  not  a  single  but  a  double  one.  There  is  in  every 
case  a  distinct  shoulder  some  distance  down  the  descent  of  the 
curve,  showing  that  the  outflow  of  blood  is  more  or  less  suddenly 
checked.  This  arrest  causes  a  wave  in  the  cardiogram  which 
may  be  well  described  as  a  recoil  wave  {vide  figs.  160, 161,  &c.) 


502  A  CASE  OF  AEHYTHMIA 

— namely,  a  wave  due  to  the  recoil  of  the  out-flowing  blood 
from  some  hindrance  which  it  experiences. 

Eecoil  waves  of  this  nature  are  of  usual  occurrence  on 
the  ordinary  systolic  cardiogram,  if  taken  a  little  to  one  side 
of  the  apex  beat  so  that  the  diminution  in  size  of  the  ventricle, 
which  results  from  the  outflow  of  its  contents,  can  be  recorded 
by  the  cardiograph.  Such  recoil  waves  show  in  the  present 
tracing.  Their  explanation  is  simple.  To  take  the  left  ven- 
tricle as  an  illustration.  In  the  normal  systole,  as  soon  as  the 
interventricular  pressure  equals  that  in  the  aorta  the  blood 
begins  to  rush  out,  and,  taking  the  direction  of  least  resistance, 
dilates  the  first  part  of  the  aorta.  But  the  momentum  of  the 
first  rush  of  blood  so  over-distends  the  vessel  that  its  elastic  re- 
coil comes  into  play,  and  the  sudden  rise  in  pressure,  so  caused, 
hinders  slightly  the  outflow  of  blood,  because  the  ventricle  has  to 
increase  its  force  so  as  to  overcome  this  increased  resistance. 
This  slight  check  to  the  outflow  often  shows  in  the  cardiogram 
as  a  distinct  wave.  There  may  be  two  or  more  of  such  waves 
to  be  seen  {vide  fig.  160,  point  3  ;  fig.  162,  point  D). 

But  to  return  to  the  extra  systole  and  its  recoil  wave. 

The  well-marked  recoil  wave  here  shown  cannot  be  due  to 
the  elastic  recoil  of  the  aorta,  for  it  has  been  demonstrated 
that  the  extra  systole  is  an  imperfect  contraction  and  does  not 
send  blood  into  the  aorta. 

Moreover,  it  is  not  due  to  a  recoil  from  an  ineffectual  attempt 
to  open  the  semilunar  valves,  because  it  occm'S  after  the 
ventricle  has  got  rid  of  a  considerable  part  of  its  contents, 
for  it  occurs  nearly  half-way  down  the  descent  of  the  curve. 

It  must,  therefore,  be  due  to  some  hindrance  to  blood  which 
is  regurgitating  through  the  auriculo-ventricular  valves  into 
the  auricle. 

We  must  now  turn  to  the  right  side  of  the  heart,  because 
here  alone  can  we  study  graphically  what  happens  to  the 
regurgitating  blood. 

But  liefore  entering  upon  the  discussion  of  the  various 
waves  in  the  venous  tracing  and  their  significance,  it  will 
be  necessary  to  point  out  that  the  argument  must  be  based 
upon  exact  correlation  of  the  waves  in  the  vein  and  in  the  apex 
tracing  by  means  of  accurate  measurements. 


WITH  EXTRA  SYSTOLES  503 

No  Delay  in  Transmission  of  impiilsos  between  the 
ventricle  and  the  vems  of  the  neck. — The  correlation  of 
venous  and  apex  tracings  by  measurements  is  only  reliable 
in  so  far  as  it  is  possible  to  allow  for  the  amount  of  delay 
that  takes  place  in  the  transmission  of  impulses  from  the 
ventricle  to  the  neck.  It  might  be  supposed  that  there  would 
be  delay  and  that,  for  instance,  the  wave  duo  to  the  auricular 
contraction  would  reach  the  jugular  vein  a  measurable  time 
after  it  show^ed  over  the  ventricle.  Measurement,  on  the  other 
hand,  shows  that  there  is  no  recognisable  delay  at  all  and  that 
the  auricular  wave  reaches  the  two  spots  practically  simul- 
taneously (figs.  161,  162).  It  must  be  remembered  that  tracings 
taken  over  what  is  called  the  jugular  bulb,  record  the 
movements  of  the  blood  which  is  enclosed  in  the  great  veins 
between  the  valves  at  the  root  of  the  neck  and  the  heart. 
Therefore,  we  can  say  that  the  tone  of  the  muscular  walls  of 
these  veins  is  so  high — in  this  case,  at  all  events — that  the 
blood  within  the  great  veins  behaves,  so  far  as  the  transmis- 
sion of  impulses  is  concerned,  as  if  it  w^ere  in  a  tube  with  rigid 
walls.  Therefore,  in  dealing  with  the  transmission  of  impulses 
from  the  heart  to  the  jugular  bulb,  no  time  allowance  need  be 
made,  and  the  transmission  maj'  l)e  considered  instantaneous. 

But  to  return  to  our  argument,  regarding  the  nature  of 
the  '  recoil  wave  '  on  the  wave  due  to  the  extra  systole.  There 
is  no  evidence  of  any  resistance  in  the  veins  which  could  cause 
this  wave.  At  the  time  of  its  occm'rence  the  veins  are  almost 
at  their  emptiest  {vide  fig.  157 ;  figs.  160  and  161,  point  8),  and 
there  is  no  sign  of  any  increased  pressure  in  them  adequate 
to  cause  such  a  hindrance  to  the  tricuspid  regm'gitation  as  is 
evidenced  l)y  this  recoil  wave.  As  a  matter  of  fact  this  recoil 
wave  exactly  corresponds  to  the  lowest  point  of  the  venous 
tracing  just  before  the  commencement  of  the  big  rise,  of  which 
we  are  about  to  speak.  We  are  therefore  driven  to  the  con- 
clusion that  the  recoil  which  causes  this  wave  must  come 
back  into  the  ventricle  from  the  amicle. 

Tonic  Contraction  of  the  walls  of  the  Auricle  during 
diastole. — This  brings  us  face  to  face  with  an  important  fact — 
for  such  it  must  be  called — namely,  that  the  auricular  walls  are 
in  a  state  of  tonic  contraction  during  the  diastole.     Now  at  the 


504  A  CASE  OF  AEHYTHMIA 

point  of  time  of  which  we  are  speaking,  the  auricle  has  just 
been  completely  emptied  into  the  ventricle,  and  therefore  ought 
to  be  relaxed  and  empty  and  able  to  receive  the  greater  part 
of  the  contents  of  the  ventricle,  without  offering  any  resistance 
to  their  reception.  The  fact  that  it  is  able  to  return  a  well- 
marked  recoil  wave  into  the  ventricle  before  the  latter  has 
half- emptied  itself  proves  that  the  auricular  walls  must  have 
contracted  down  as  the  blood  passed  out  of  it,  and  must  remain 
in  a  state  of  tonic  contraction  and  resent  the  entrance  of  the 
blood  regurgitating  from  the  ventricle.  Now  the  main  wave 
in  the  neck  of  which  we  are  speaking  commences  immediately 
after  the  return  into  the  ventricle  of  this  recoil  wave  from  the 
auricle,  and  its  maximum  rise  corresponds  to  the  minimal  fall 
of  the  apex  tracing  {vide  figs.  160  and  161,  point  9 ;  and  Plate  X). 
It  is  quite  evident  from  the  tracing  that  this  increase  in  the 
fullness  of  the  vein  coincides  with  the  emptying  of  the  ventricle, 
and  is  therefore  due  to  tricuspid  regurgitation,  the  blood  being 
diverted  from  the  auricle  into  veins  by  the  resistance  offered 
by  the  muscular  tone  of  the  auricular  walls.  If  the  large 
wave  in  the  vein  had  been  due  to  an  am'icular  contraction 
there  would  have  been  a  wave  in  the  ventricular  tracing 
synchronous  with  that  in  the  vein. 


Sudden  Distension  a  Cause  of  an  Auricular 
Contraction 

In  confirmation  of  what  has  just  been  said  there  is 
evidence  that  such  an  auricular  contraction  does  take  place 
occasionally. 

In  some  of  the  heart  beats  the  even  descent  of  the  cm've, 
as  the  ventricle  empties  itself  dm'ing  the  extra  systole,  is 
broken  by  a  wave  showing  a  sudden  increase  of  pressure  such 
as  would  be  caused  by  an  auricular  contraction  (fig.  161, 
point  a).  In  the  beats  where  this  occm's  the  big  rise  in  the 
vein  is  broader  and  more  sustamed  than  where  it  does  not 
occur  (Plate  X).  The  appearance  of  these  two  synchronous 
waves  may  be  taken  as  proof  that  an  auricular  contraction 
occurred  at  this  point  {vide  fig.  161,  point  o;   and  Plate  X). 


WITH  EXTRA  SYSTOLES  505 

The  cause  of  this  auricular  contraction  is  clear.  The  hindrance 
offered  to  the  regurgitation  by  the  auricular  walls  (to  which 
the  recoil  wave  is  due)  requires  a  slight  increase  in  the  ex- 
pulsive force  of  the  ventricle  in  order  to  overcome  it.  This 
sudden  increase  in  the  expulsive  force  of  the  ventricle  seems 
in  some  instances  to  be  too  much  for  the  resisting  power  of 
the  auricular  walls  and  therefore  stimulates  them  to  contract. 
This  tracing  seems  clearly  to  show  that  the  sudden  stretch- 
ing of  the  auricular  walls  which  this  extra  effort  of  the 
ventricle  occasions,  does  stimulate  the  auricle  to  a  true 
contractile  act.  In  confirmation  of  this,  it  will  be  noticed 
that,  in  those  beats  where  this  extra  auricular  systole  occurs, 
the  extra  ventricular  systole  is  more  powerful  (if  we  may 
judge  it  by  the  height  of  its  wave  in  the  cardiogram)  than  in 
those  beats  where  it  does  not  occur.  Note  the  relative  size  of 
the  rise  due  to  the  extra  sj^stole  in  the  two  types  of  beat  in 
figs.  160  and  161  and  Plate  X. 

But  even  in  the  case  of  these  stronger  beats  the  auricular 
contraction  does  not  cause  the  rise  in  the  venous  tracing,  but 
only  augments  the  rise  which  the  tricuspid  regm'gitation  is 
already  causing.  In  those  beats  where  there  is  certainly  no 
auricular  contraction  the  big  wave  in  the  veins  is  as  Mgh, 
though  not  so  broad,  as  those  where  the  auricle  does  contract. 
The  tracings,  therefore,  show  that  this  rise  in  the  venous  pulse 
is  of  ventricular  and  not  of  auricular  origin. 

Oscillation  of  Blood  Backwards  and  Forwards 
BETWEEN  Veins  and  Auricle. — In  those  beats  where  the 
blood,  regurgitating  into  the  auricle,  has  not  sufficient  force 
to  overcome  the  tonic  resistance  of  the  auricular  wall,  there 
are  other  phenomena  to  bo  noticed  {vide  fig.  160  and  Plate  X). 
In  these  beats  it  seems  as  if  the  blood  were  not  driven  into 
the  veins  with  sufiicient  force  to  overcome  the  tonic  resistance 
of  their  muscular  walls  and  therefore  this  tonic  resistance  was 
able  to  throw  the  regurgitating  blood  back  once  more  into 
the  ventricle  with  sufficient  force  to  make  a  very  distinct  rise 
in  the  ventricular  tracing.  Careful  comparison  of  the  venous 
and  the  ventricular  tracings  shows  how  exact  is  the  corre- 
spondence between  the  fall  in  the  venous  tracing  and  the  rise 
in  the  apex  cardiogram,  and  vice  versa.     The  wave  seems  to 


506  A  CASE  OF  ARHYTHMIA 

oscillate  backwards  and  forwards,  between  the  ventricle  and 
the  veins,  before  it  finally  dies  down  {vide  fig.  160,  points  10, 
15,  16). 

In  those  beats  where  a  true  auiiciilar  contraction  occurs, 
this  oscillation  of  the  blood  wave  is  not  seen.  The  reason 
probably  is  that  the  auricular  contraction  raises  the  blood 
pressure  in  the  vein — ^just  as  it  is  commencing  to  contract — 
to  an  extent  sufficient  to  prevent  the  vein  from  emptying 
itself  into  the  ventricle.  Note  that  the  wave  in  the  vein 
which  results  from  the  auricular  contraction  checks  the  fall 
which  is  due  to  the  commencement  of  the  venous  contrac- 
tion. This  is  well  shown  in  the  third  beat  from  the  right- 
hand  end  of  the  tracing  shown  in  Plate  X.  It  will  be 
noticed  that  the  larger  beats,  where  the  amicular  contraction 
occurs,  often  alternate  with  smaller  ones  where  there  is  none 
and  where  two  other  waves  follow  the  extra  systole  in  the 
apex  tracing  and  one  in  the  venous  tracing. 

Contraction  of  the  Veins. — In  the  smaller  beats,  already 
spoken  of,  the  big  wave  in  the  veins  has  another  character- 
istic besides  its  relative  narrowness.  If  it  be  compared  with 
the  alternate  broader  ones  it  will  be  seen  that  the  emptying  of 
the  vein  is  more  sudden  and  that  the  fall  is  often  continued 
below  the  base  level.  Both  these  features  imply  a  degree  of 
suddenness  which  points  to  the  occm'rence  of  a  triie  con- 
traction of  the  vein.  It  is  not  unusual  to  observe,  in  venous 
tracings,  phenomena  such  as  these,  which  seem  to  point 
clearly  to  the  occurrence  of  true  contraction  of  the  veins.  The 
occurrence  of  this  contraction  in  the  veins  cannot  be  recorded 
graphically  except  under  certain  conditions — ^namely,  the  dis- 
tension of  the  vein,  while  being  sudden  enough  to  produce  a 
well-marked  contraction,  must  not  be  so  great  as  to  overpower 
the  muscles  of  the  veins,  nor  so  prolonged  that  the  stimulus 
to  contract  has  time  to  pass  off  and  thus  lose  its  effect, 
before  the  pressm-e  is  sufficiently  lowered  to  admit  of  the  con- 
traction emptying  the  vein.  In  the  beats  where  the  extra 
auricular  systole  occurred  these  two  conditions  were  not 
fulfilled  and  no  evidence  of  any  contraction  of  the  veins  is 
visible. 

Wave  in  Ventricular  Tracing  due  to  a  Eeturn  Wave 


WITH  EXTRA  SYSTOLES  507 

FROM  THE  Veins. — Where,  however,  this  effective  contraction 
of  the  vehis  does  occur,  the  blood  is  returned  towards  the 
ventricle  with  sufficient  force  to  cause  the  second  rise  in  the  apex 
cardiogram  of  which  we  have  been  speaking. 

On  looking  at  this  second  rise  {vide  fig.  160,  points  1(3.  11, 
and  12).  it  will  be  noticed  that  the  upstroke  is  rather  a  gradual 
one,  and  sometimes  there  are  two  more  or  less  distinct  waves — 
one  on  the  upstroke,  and  one  constituting  the  apex  of  the  rise. 
The  first  of  these  two  waves  is  synchronous  with  the  emptying 
of  the  vein,  and  is  due  to  the  impact  upon  the  ventricle  wall  of 
the  blood  sent  into  it  by  the  venous  contraction.  The  second 
is  synchronous  with  a  small  wave  in  the  venous  pulse.  This 
wave  must  be  of  auricular  origin  and  produced  by  the  tonic 
response  of  its  walls  to  the  blood  sent  into  it  from  the  veins. 
When  the  veins  contract,  the  blood  is  thrown  into  both 
auricle  and  ventricle,  but  the  tonic  response  of  the  auri- 
cular wall  sends  it  out  again  in  both  directions,  and  so 
causes  both  the  small  wave  in  the  vein  and  the  highest  point 
of  the  rise  due  to  the  filling  of  the  ventricle  {vide  fig.  IGO, 
point  12). 

Sensitiveness  of  Veins  and  Auricle  to  Sudden 
ChanCtES  of  Pressure. — There  are  one  or  two  other  facts 
which  testify  to  the  sensitiveness  of  the  auricle  and  the 
great  veins  to  -sudden  variations  of  pressure  within  them, 
and  to  the  speedy  passage  of  waves  to  (and  in)  them,  owing 
to  the  tonic  contraction  of  their  walls.  For  instance,  at  the 
time  of  occurrence  of  the  maximal  fullness  of  the  vein,  during 
the  tricuspid  regurgitation,  there  is  a  small  oscillation  over 
the  ventricle  synchronous  with  the  apex  of  the  venous  rise, 
showing  that  the  increase  of  tension  due  to  the  venous 
distension  shows  itself  in  the  ventricle  {vide  fig.  160,  point  9  ; 
and  Plate  X). 

Again,  there  is  sometimes  a  small  oscillation  in  the  vein 
synchronous  with  the  commencement  of  the  extra  systole,  as  if 
the  rush  of  blood  from  the  ventricle  into  the  auricle  caused  a 
slight  disturbance  in  the  intravenous  pressure  ;  but,  as  it 
found  fairly  free  entry  into  the  auricle,  a  more  marked  wave 
was  not  caused  in  the  vein. 

I  think  I  have  now  given  abundant  evidence  to  prove  the 


508  A  CASE  OF  ARHYTHMIA 

thesis  I  set  out  to  prove — namely,  '  that  throughout  the 
diastole  the  blood  in  the  auricles  and  great  veins  is  main- 
tained— in  this  case,  at  all  events — at  a  definite  degree  of 
tension  by  the  muscular  walls  of  both  auricle  and  veins, 
and  that  their  walls  are  so  sensitive  as  to  respond  at  once 
by  increased  tonic  activity  or  by  definite  contraction  to  any 
sudden  tendency  to  alteration  of  the  blood  pressure  within 
them.' 

This  tracing  also  seems  to  show  that  the  veins  are  stimu- 
lated to  contract  by  any  sudden  lessening  of  the  blood  pressure 
within  them.  The  deepness  and  suddenness  of  the  emptying, 
which  takes  place  after  the  normal  auricular  systole  (during 
what  is,  presumably,  its  time  of  elastic  recoil  or  active  expan- 
sion), seems  to  show  that  a  true  venous  contraction  occurs 
here. 

Additional  Evidence. — When  this  patient  was  taking 
aconite,  and  the  extra  systole  was  prevented,  in  most  of 
the  beats,  by  the  lessening  of  the  expansile  force  of  the 
ventricle,  there  was,  nevertheless,  evidence  that  the  ven- 
tricle was  still  somewhat  over-distended  by  its  own  expansile 
force. 

In  fig.  162,  point  e,  it  will  be  seen  that  the  slight  depression 
in  the  venous  tracing  which  corresponds  to  the  aspiration 
period  of  the  ventricle  is  immediately  followed  by  a  slight 
filling  up  of  the  vein.  This  shows  clearly  that  the  blood  not 
only  rushes  into  the  right  ventricle  during  its  expansion,  but 
also  that  it  more  than  fills  it,  and  that  some  passes  out  again 
into  the  veins — as  the  result,  presumably,  of  the  elastic  recoil 
of  the  over-distended  ventricle.  In  this  tracing,  however,  the 
over-distension  is  not  sufiicient  to  stimulate  the  ventricle  to 
contract  and  cause  an  extra  systole.  In  this  tracing,  when 
the  extra  systole  does  occur  it  causes  only  a  small  wave  in  the 
veins  of  the  neck,  and  some  of  the  blood  therefore  must  either 
simply  return  into  the  auricle,  or  else,  in  this  case,  the  ventricle 
must  succeed  in  sending  some  blood  into  the  pulmonary  artery 
and  aorta.  Of  these  two  hypotheses,  I  think  the  latter  the  more 
probable,  although,  unfortunately,  I  have  not  a  carotid  tracing 
whereby  to  verify  it.  This  supposition  that  the  extra  systole 
does  pass  some  blood  through  the  semilunar  valves  is  confirmed 


WITH  EXTRA  SYSTOLES  509 

by  the  character  of  the  succeeding  ordinary  systole,  for  its 
commencement  is  delayed  and  it  also  does  less  work  than  usual, 
so  far  as  can  be  judged  from  the  breadth  of  the  systolic  rise  in 
the  cardiogram. 

Careful  measurements  of  the  amount  of  delay  of  the  start 
of  the  systole  as  compared  with  the  dela}''  in  the  time  of  occur- 
rence of  the  second  aortic  recoil  waves,  brings  out  an  interesting 
fact — namely,  although  the  start  is  delayed  to  the  extent  of 
nearly  one-eighth  of  the  normal  interval  (i.e.  more  than  11| 
per  cent.),  the  time  of  occm-rence  of  the  second  aortic  recoil 
wave  is  only  delayed  less  than  one-sixteenth  of  the  normal 
interval  (i.e.  6  per  cent.)  {vide  fig.  162).  This  observation  shows 
that  although  the  commencement  of  this  systole  is  much 
delayed,  nevertheless  it  fills  the  aorta  very  quickly.  This  must, 
I  think,  be  taken  as  evidence  that  the  extra  systole  had  already 
thrown  some  blood  into  the  aorta  and  partly  filled  it.  In  this 
way  the  extra  systole,  and  the  normal  systole  following  it, 
together  make  up  one  normal  beat.  Moreover,  there  is  no 
lasting  interference  with  the  cardiac  rhythm,  for  the  next 
beat  after  the  extra  systole  occurs  at  the  time  it  would 
have  done  had  there  been  no  extra  systole.  (See  also  the 
explanatory  notes  to  fig.  162.) 

Prolonged  Auricular  Contraction  in  Tricuspid  Ee- 
GURGiTATioN. — Tliis  theory  of  the  tenseness  and  sensitiveness 
of  the  auricles  and  veins  is  also  supported  by  the  only  tracings 
that  I  have  been  able  to  obtain  from  the  right  auricle 
itself.  These  showed  that  the  auricle  was  drawn  away  from 
the  chest  wall  during  its  own  systole  and  remained  in  the  same 
state  until  nearly  the  end  of  the  ventricular  systole.  But  the 
interesting  point  was  that  the  systolic  wave  which  showed  in 
the  ventricular  cardiogram  was  reflected  in  miniatme  in  the 
contracted  auricle,  making  the  portion  of  the  auricular  tracing 
which  corresponded  to  the  ventricular  sj^stole  resemble  the 
ventricular  one  to  some  extent.  I  could  not  understand  this 
at  the  time  (namely,  in  1892) ;  but  now  it  is  plain,  for  I  know 
that  the  auricle  is  sensitive  to  every  change  in  pressure  that 
takes  place  in  the  ventricle  {vide  Plate  XII). 


510  A  CASE  OF  ARHYTHMIA 

Tonic  Activity  of  the  Ventricular  Walls  during 

THE    '  KeLAXATION  '    PhASE  (?) 

These  tracings  also  seem  to  demonstrate  the  fact  that 
the  wall  of  the  right  ventricle  is  not  in  a  state  of  passivity 
durmg  its  relaxation  phase,  but  is  in  a  state  of  tonic  activity, 
and  sensitive  to  mechanical  stimulation  by  any  sufficiently 
sudden  increase  of  pressure  within  it.  The  oscillation  of  blood 
between  the  vems  and  the  ventricle  which  has  just  been 
spoken  of,  inight  be  explicable  on  the  supposition  that  the  blood 
is  returned  from  the  ventricle  back  into  veins  by  its  elastic 
recoil  after  an  over-distension  due  to  the  venous  contraction. 

As  the  venous  contraction  is  sufficiently  powerful  to  distend 
the  ventricle  (see  point  No.  11  in  the  ventricular  tracing, 
fig.  160),  this  is  a  possible  supposition.  Nevertheless,  the 
suddenness  of  the  fall,  due  to  the  emptying  of  the  ventricle, 
suggests  that  the  more  probable  explanation  is  that  the 
ventricle  possesses  tonic  activity.  The  possession  of  tonic 
activity  having  been  proved  in  the  case  of  the  auricle  renders 
probable  its  possession  of  the  ventricle  also.  Further  study, 
however,  is  necessary  before  this  point  can  be  considered  to 
be  proved. 

This  possession  of  tonic  activity  by  the  left  ventricle,  during 
its  relaxation  phase,  is  also  suggested  by  the  suddenness  of  its 
emptying  when  over-distended  by  its  own  aspiration  under  the 
conditions  described  in  Essay  XII,  and  illustrated  by  the 
tracmgs  shown  in  the  figures  on  pp.  433,  434,  437,  438.  More- 
over, the  tracings  shown  on  pp.  432  and  433  show  waves 
following  the  suction  recoil  wave,  which  are  almost  certainly 
due  to  the  oscillation  of  the  blood  backw^ards  and  forwards 
between  the  left  auricle  and  left  ventricle. 

The  explanation  of  the  extra  systole,  which  this  case  gives, 
throws  much  light  upon  the  occurrence  of  this  type  of  nregu- 
larity  in  valvular  disease.  This  type  of  extra  systole  is  a  very 
common  one,  and  it  is  highly  probable  that  when  it  occurs 
it  shows  that  the  ventricle  is  being  over-distended  by  its  own 
expansile  force.  Certainly,  over-distension  is  likely  to  occur 
in  an  embarrassed  heart  with  a  dilated  auricle,  such  as  is 
frequent  in  valvular  disease. 


WITH  EXTRA  SYSTOLES  511 

Further  consideration  of  this  and  similar  cases  will,  I  have 
no  doubt,  bring  out  the  fact  that  the  inception  of  cardiac 
contraction  is  not  such  a  purely  spontaneous  function  of  the 
various  nodes  as  some  writers  seem  to  think,  but  that  the 
occurrence  of  cardiac  contraction  may  also  often  be  of  the 
nature  of  a  reflex  act,  the  afferent  impulses  being  caused 
by  the  distension  and  stretching  of  the  cardiac  walls.  It 
is  probable  that  the  occurrence  of  reflex  cardiac  contrac- 
tion will  be  proved  before  long  by  means  of  the  electric 
cardiograph. 


512  A  CASE  OF  ARHYTHMIA 

EXPLANATIONS  OF  THE  TRACINGS 

Fig.  160. 

Two  portions  of  the  tracing  given  in  Plate  X  are  here  shown.  Each  portion 
includes  a  single  normal  ventricular  contraction  with  an  e^ctra  systole  and 
the  wave  due  to  the  return  of  blood  to  the  ventricle  again  from  the  veins. 

In  each  portion,  the  ventricular  and  the  venous  tracing  are  correlated  by 
means  of  tliin  vertical  lines  connecting  the  corresponding  points  of  the  two 
tracings.  These  lines  are  copied  from  the  original  tracing  in  which  the  points 
in  the  ventricular  and  the  venous  tracing  were  very  accurately  ascertained. 
The  tracing  given  in  Plate  X  will  enable  anyone,  who  is  desirous  of  doing  so, 
to  verify  this  statement  by  actual  measurements. 

In  the  first  portion  the  main  events  recorded  are  indicated  in  words. 

In  the  second  portion  another  similar  beat  is  shown,  but  the  various  distinct 
events  are  each  numbered,  in  order  that  they  may  be  described  in  detail, 
as  follows : — 

1.  The  final  rise  of  the  auricular  wave  in  the  vein  is  shown  to  be  exactly 
synchronous  with  the  commencement  of  the  ventricular  systole — showing 
no  delay  in  the  transmission  of  the  auricular  wave  to  the  jugular  bulb,  over 
which  the  venous  tracing  was  taken. 

2.  The  highest  point  of  the  ventricular  systoUc  rise  is  shown  to  correspond 
with  the  deepest  point  of  the  notch  which  follows  the  auricular  wave  in  the 
vein.  In  this  particular  beat  the  suddenness  of  the  drop  shows  that  there 
was  very  rapid  emptying  of  the  vein.  This  sudden  drop  in  the  tracing  suggests 
that  an  actual  contraction  took  place  in  the  vein,  and  supports  the  theory 
that  the  relief  of  tension  which  occurred  as  the  blood  rushed  into  the  auricle 
(as  it  expanded  after  its  systole)  was  sufficiently  sudden  to  cause  a  true 
contraction  of  the  walls  of  the  vein. 

3.  The  first  aortic  recoil  wave — due  to  the  check  which  the  blood  flowing 
out  of  the  ventricle  receives  when  the  first  part  of  the  aorta  is  fully  distended. 
This  point  coincides  with  the  highest  point  of  the  systolic  rise  in  the  vein. 
This  fact  seems  to  prove  that  the  systohc  rise  in  the  vein  is — in  this  patient, 
at  all  events — due  to  the  compression  of  the  superior  vena  cava  by  the  over- 
distension of  the  first  part  of  the  aorta.  (This  aortic  recoil  wave  does  not 
show  very  clearly  in  this  beat,  but  it  does  show  in  the  first  beat  given  in  this 
figure.) 

4.  The  second  aortic  recoil  wave.  This  wave  appears  to  be  due  to  the 
hindrance  to  the  outflow  of  blood  from  the  ventricle,  which  results  when  all 
the  main  arteries  are  distended  and  the  elasticity  of  their  walls  begins  to  come 
into  play,  and  thus  necessitates  a  final  expulsive  effort  on  the  part  of  the 
ventricle. 

This  second  recoil  wave  is  more  often  evident  upon  the  ventricular  tracing 
than  is  the  case  with  the  first. 

In  the  venous  tracing  this  recoil  wave  often  coincides  with  the  point  where 
the  fall  due  to  the  emptying  of  the  vein  after  its  systolic  fullness  comes  to 
an  end. 

According  to  the  theory  just  giv^en  as  to  the  cause  of  the  systolic  rise  in 
the  venous  tracing,  this  is  to  be  expected ;  for  the  fall  is  due  to  the  relief  of 
pressure  On  the  superior  vena  cava  which  accompanies  the  emptying  of  the 
first  part  of  the  aorta  as  its  elastic  recoil  comes  into  play,  and  the  return  of 
blood  towards  the  heart  from  the  distant  arteries  will  again  increase  the  amount 


WITH  EXTRA  SYSTOLES 


513 


Apex 

trdLcing- 


Veiioua 
tracing- 


Fig.   160. 


of  distension  of  this  part  of  the  aorta  and  so  tend  once  more  to  compress  the 
superior  vena  cava  somewhat. 

5.  This  wave  in  the  ventricular  tracing  marks  the  time  of  occurrence 
of  the  second  sound  of  the  heart  and  the  commencement  of  the  expansion 
phase. 

In  the  vein  it  sometimes  coincides  with  a  somewhat  sudden  drop  due  to  an 
emptying  of  the  vein  at  the  time  when  the  blood  is  being  aspirated  from  the 
auricle  into  the  ventricle.     Tliis  is  shown  in  fig.  161. 

More  often,  however,  in  this  particular  case,  the  fullness  of  the  jugular 
bulb  does  not  appear  to  be  materially  lessened  at  the  time  of  the  ventricular 
aspiration  {vide  fig.  162). 

6.  Marks  the  lowest  point  of  the  ventricular  tracing  and  the  termination 
of  the  expansion  phase. 

2l 


514  A  CASE   OF  ARHYTHMIA 

In  the  normal  beat  it  marks  the  point  where  relajcation  commences,  but 
here  it  marks  tlic  commencement  of  an  abnormal  contraction — namely,  the 
extra  systole. 

In  many  of  the  tracings  this  point  falls  part-way  up  a  small  rounded  rise 
in  the  venous  tracing.  It  will  be  remembered  that  we  are  dealing  here  with 
a  case  in  which  the  ventricle  is  presumably  aspirating  more  blood  towards 
itself  than  it  can  well  hold.  A  certain  amount  of  this  blood  may  therefore 
be  expected  to  escape  from  the  ventricle  again  when  the  elasticity  of  the 
ventricle  wall  comes  into  play.  Such  a  return  of  blood  from  the  ventricle 
into  the  veins  probably  causes  the  small  rounded  rise  in  the  venous 
tracing,  at  the  commencement  of  the  relaxation  phase,  of  which  we  are 
now  speaking. 

7.  The  highest  point  of  the  rise  in  the  ventricular  tracing  which  is  due  to 
the  extra  systole.  In  the  vein,  this  corresponds  to  the  highest  point  of  the 
rounded  rise  just  referred  to. 

8.  The  recoil  wave  which  causes  a  break  in  the  fall  of  the  ventricular  tracing 
after  the  rise  due  to  the  extra  systole.  This  must  be  due  to  some  check  to 
the  outflow  of  blood  (as  pointed  out,  p.  503).  It  must  be  due  to  the  tonic 
contraction  of  the  walls  of  the  auricle  which  is  caused  by  the  inrush  of  blood 
from  the  ventricle.  This  recoil  wave  is  shown  to  correspond  with  the  lowest 
point  of  the  venous  tracing  just  before  the  big  rise. 

9.  This  is  the  lowest  point  of  the  ventricular  tracing,  and  corresponds  to 
the  highest  point  of  the  big  rise  in  the  venous  tracing  which  is  due  to  the  dis- 
tension of  the  veins  by  the  blood  which  enters  them  as  the  result  of  the  extra 
systole. 

In  this  tracing,  as  pointed  out  at  p.  505,  it  appears  that  the  tonic  response 
of  the  walls  of  the  auricle  drives  the  blood  which  has  entered  it  out  again 
into  the  veins. 

10.  Marks  the  foot  of  the  fall  due  to  the  emptying  of  the  vein  after  its 
distension. 

Here  the  fall  is  sudden  enough  to  suggest  a  true  contraction  of  the  walls 
of  the  vein,  their  sudden  over-distension  presumably  stimulating  the  muscles 
of  their  walls  to  a  true  contraction.  The  emptying  of  the  vein  coincides  with 
a  re-filling  of  the  ventricle  {vide  point  10  on  the  ventricular  tracing). 

11.  At  the  point  11,  a  further  rise  takes  place  in  the  ventricular  tracing, 
and  this  also  coincides  with  a  rise  of  the  venous  tracing.  This  sudden 
slight  fining  of  both  vein  and  ventricle  must  be  due  to  auricular  activity, 
and  the  ejcplanation  is  that  the  inrush  of  blood  into  the  auricle  caused  a  tonic 
muscular  response,  and  this  drove  the  blood  out  again  into  both  vein  and 
ventricle. 

12.  The  maximal  point  of  this  rise  in  both  vein  and  ventricle. 

13.  The  ventricular  rise  due  to  this  return  of  the  blood  from  the  veins  now 
suddenly  subsides  and  the  blood  is  once  more  driven  back  into  the  veins, 
but  with  lessened  force. 

After  this  there  is  a  slight  return  once  more  to  the  ventricle,  and  sometimes 
another  wave  shows  in  the  vein  before  the  oscillation  of  blood  between  the 
ventricle  and  the  jugular  bulb  finally  subsides. 

15.  Marks  the  lowest  point  in  the  ventricular  tracing  and  corresponds 
to  a  slight  crest  in  the  vein,  and,  again— 

16.  Marks  the  reverse,  a  slight  crest  in  the  ventricle  tracing,  corresponding 
to  a  slight  depression  in  the  venous  one. 


WITH  EXTRA  SYSTOLES 


515 


Vein 


Fig.  161. 

This  is  another  portion  of  the  tracing  given  in  Plate  X. 

The  explanation  given  of  fig.  160  also  applies  to  this  figure  up  to  point  9. 

At  9  in  tliis  tracing  the  fall  of  the  tracing  as  the  ventricle  empties  itself 
at  the  end  of  the  extra  systole  is  checked  by  the  occurrence  of  a  fairly  sharp 
wave  with  a  rounded  top.     (Wave  (a).) 

(a)  This  is  due  to  a  distension  of  the  ventricle  by  a  true  contraction  of  the 
auricle,  the  result  of  its  sudden  distension  by  the  regurgitation  which  the  extra 
systole  causes. 

Note  that  in  the  beats  where  this  auricular  contraction  occurs  the  extra 
systole  (as  judged  by  the  tracing)  is  more  powerful  than  in  beats  (such  as  those 
shown  in  fig.  160)  where  there  is  no  auricular  contraction. 

In  the  jugular  bulb  tracing  there  is  a  broadening  of  the  wave  when  this 
auricular  contraction  occurs  (see  Plate  X). 

(b)  The  lowest  point  of  the  ventricular  tracing  corresponds  to  an  increase  in 
the  distension  of  the  vein  (as  judged  by  a  broadening  of  the  big  rise  in  the 
venous  tracing)  as  the  blood  which  the  auricle  sent  into  the  ventricle  is  again 
sent  out  of  it  into  the  vein. 


5J6  A  CASE  OF  AEHYTHMIA 

(r)  This  is  a  small  pointed  wave  in  the  ventricular  tracing  which  corresponds 
to  the  iinal  emptying  of  the  vein  after  the  big  rise  clue  to  its  distension  by  the 
extra  systole.  The  fact  that  no  wave  in  the  vein  accompanies  it  negatives 
the  possibihty  that  it  is  due  to  a  return  of  blood  back  from  the  auricle,  and 
the  fact  that  no  further  oscillations  take  place  after  it  points  to  its  being  an 
expansion  of  the  ventricle  following  the  contractile  effort  which  caused  the 
sudden  drop  after  wave  («). 

Fig.    162 

This  is  a  portion  of  Tracing  No.  G,  Plate  XI,  which  has  already  been 
referred  to  at  p.  508,  and  which  shows  tracings  taken  while  the  patient  was 
under  the  influence  of  aconite.  The  upper  tracing  was  taken  from  the  cardiac 
apex,  and  the  lower  from  the  jugular  bulb.  Corresponding  points  upon  the 
tracings  are  connected  by  thin  vertical  lines.  The  length  of  time  intervening 
between  various  points  of  the  tracing  in  each  successive  beat  is  shown  (in 
decimals  of  a  second)  by  the  figures  upon  the  thin  horizontal  lines  drawn 
between  those  points. 

The  following  facts  are  to  be  noted  : — 

1.  There  is  no  well-marked  wave  in  the  vein,  directly  due  to  the  ventricular 
extra  systole,  such  as  is  shown  in  figs.  157,  160,  161.  If  present  it  ought  to 
occur  at  point  A. 

2.  The  narrowness  of  the  ventricular  rise  in  the  apex  tracing,  due  to  the 
systole  wliich  follows  the  extra  systole — i.e.  point  B.  This  may  be  due  to 
exhausted  excitability,  or  to  some  blood  having  been  passed  into  the  aorta 
by  the  extra  systole,  thus  leaving  less  than  the  normal  amount  of  work  for 
the  ordinary  ventricular  systole  to  do. 

3.  The  rise  in  the  venous  tracing  which  corresponds  to  this  same  ventricular 
systole  takes  place  later  than  usual,  and  it  corresponds  to  the  second  aortic 
recoil  wave  instead  of  the  first,  as  is  the  case  normally.  Compare  point  C  with 
point  D. 

According  to  the  theory  here  given  as  to  the  cause  of  the  systolic  rise  in 
the  vein,  this  lateness  of  the  rise,  in  this  instance,  points  to  the  first  part  of  the 
aorta  not  being  fully  distended  in  the  early  portion  of  the  ventricular  systole, 
but  to  its  full  distension  at  the  time  of  the  second  aortic  recoil  wave.  This 
might  be  expected  to  occur  when  (as  is  probably  the  case  in  this  particular 
beat)  the  ventricle  contains  less  blood  than  normal,  owing  to  some  blood 
having  been  already  passed  on  into  the  aorta  by  the  extra  systole. 

4.  The  wave  in  the  vein  which  occurs  at  the  end  of  the  ventricular  ex- 
pansion period  (point  E  on  the  tracing),  and  is  due  to  a  reflux  of  blood  from 
the  ventricle  (consequent  upon  its  overfilUng  itself  during  its  expansion  period) 
is  smaller  when  the  extra  systole  occurs  than  in  the  normal  beats.  The  ex- 
planation of  this  is  to  be  found  in  the  fact  that  the  extra  systole  is,  in  this 
instance,  an  effective  contraction,  closing  the  auriculo-ventricular  valves  at 
the  termination  of  the  expansion  period  and  passing  the  ventricular  contents 
— in  part,  at  all  events — through  the  semilunar  valves  (i.e.  the  ventricle  in 
this  beat  has  less  blood  to  deal  writh,  it  is  less  overfilled  by  its  own  aspiration, 
and  there  is,  consequently,  less  reflux  into  the  veins  afterwards). 

5.  The  vein  shows  a  greater  degree  of  emptying  than  normal  during  the 
expansion  period  of  the  beat  which  follows  the  extra  systole.  This  is  evident 
on  comparing  the  point  F  with  the  tracing  ju.st  before  the  point  E  in  the 
preceding  beats. 

The  explanation  of  tliis  is  to  be  found  in  the  fact  that,  the  ventricle  being 


WITH  EXTRA  SYSTOLES 


5J7 


i 


f^'  ft 


Fig.   102. 


imperfectly  filled,  its  beat  will  end  more  suddenly  than  normal.  This  will 
increase  the  force  of  its  expansion  and  thus  draw  more  blood  than  usual  from 
the  auriculo-venous  reservoir. 

6.  The  wave  in  the  vein,  due  to  the  return  of  blood  fi'ora  the  ventricle, 
at  the  end  of  the  expansion  period  is  higher  than  normal  in  the  beat  following 
the  extra  systole.  Compare  the  height  of  the  wave  at  the  point  H  with  the 
two  preceding  beats  at  the  point  marked  E. 

This  is  due  to  the  increased  aspiratory  force  spoken  of  in  paragraph  5. 
The  abnormal  amount  of  blood  drawn  towards  the  ventricle  will  cause  an 
abnormally  high  wave  when,  on  failing  to  gain  entrance  into  the  ventricle, 
it  returns  back  into  the  vein. 

The  wave  K  in  this  tracing  is  of  somewhat  doubtful  origin. 

In  the  first  place  it  occurs  at  the  time  an  ordinary  auricular  wave  in  the 
vein  is  to  be  expected,  as  shown  by  the  measured  distances  on  the  tracing. 
Moreover,  a  precisely  similar  wave  in  the  vein,  which  occiu-s  in  the  tracing 
shown  in  Plate  IX,  No.  4,  is  synclironous  with  the  '  auricular  wave  '  in  the 
apex  tracing,  and  must,  therefore,  be  coasidered  for  certain — in  part,  at  all 
events — an  auricular  wave. 


518  A  CASE  OF  ARHYTHMIA 

J 11  the  incHciil  installer,  on  tlic  ullur  hand,  tliis  wave  K  occurs  a  measurable 
time  before  the  next  ventricular  systole,  and,  also,  there  {5  in  the  ventricular 
cardiogram  evidence  of  an  auricular  wave  bearing  the  normal  relationship  to 
the  systolic  rise  B. 

If  must,  therefore,  be  admitted  that  this  rise  K  precedes  the  auricular 
systole,  and,  also,  that  in  this  particular  beat  the  auricular  sysfole  does  not 
cause  a  wave  in  the  veins  of  the  neck. 

There  are  two  factors  wliich  may  assist  in  explaining  this  somewhat  unusual 
phenomenon  of  an  auricular  systole  being  unaccompanied  by  a  wave  in  the 
jugular  bulb. 

Firstly,  the  vein  is  just  contracting  down  in  the  act  of  expelling  the  blood 
which  caused  the  rise  K,  and  its  muscular  tone  must,  therefore,  be  high  at  this 
particular  moment ;  and,  secondly,  there  is  less  blood  than  usual  for  the  auricle 
to  deal  with  and  the  ventricle  is  less  full  than  normal,  and,  therefore,  the 
auricular  contraction  will  have  to  develop  less  force  than  normal.  These 
two  factors  may  be  sufficient  to  explain  the  absence  of  a  distension  of  the 
jugular  bulb  at  the  time  of  the  auricular  systole. 

With  regard  to  the  work  done  by  the  extra  systole  in  this  type  of  tracing, 
evidence  is  given  by  the  latter  part  of  Tracing  No.  4,  Plate  IX,  which  confirms 
the  statement  that  the  extra  systole  does  throw  some  blood  back  through  the 
tricuspid  valve  (into  the  auricle  or  the  veins  or  both)  as  well  as  some  blood 
forwards  into  the  pulmonary  artery,  and  that  what  is  apparently  a  normal 
auricular  wave  in  the  vein  must — in  part,  at  all  events — be  due  to  tricuspid 
regurgitation. 

In  the  earlier  part  of  Tracing  No.  4,  Plate  IX,  the  '  auricular '  wave, 
which  is  nearly  .synchronous  with  the  eiid  of  the  extra  systole,  is  but  little 
larger  than  is  usual  in  this  type  of  tracing.  Tliis  is  so  in  the  portion  of  No.  6, 
which  is  copied  to  make  fig.  162.  In  the  second  extra  systole  of  No.  4, 
however,  the  wave  in  the  vein  is  decidedly  high. 

At  the  end  of  No.  4  the  type  of  beat  changes  and  the  heart  adopts  a  new 
rhythm,  in  which  an  e?tra  systole  follows  each  beat. 

Now  in  the  last  beat,  prior  to  the  adoption  of  the  new  rhythm,  an  extra 
systole  occurs  which  is  similar  in  all  respects  to  those  seen  in  the  earher  part 
of  the  tracing  and  the  interesting  point  is  that  this  extra  systole  is  accompanied 
by  the  wave  K  in  the  vein  (of  which  we  have  just  been  speaking),  although 
there  is  no  succeeding  ventricular  systole  and  no  evidence  of  any  auricular 
contraction.  Therefore,  this  particular  beat  suggests  that  tricuspid  regurgita- 
tion does  play  an  important  part  in  the  production  of  tliis  wave  K,  which 
would  ordinarily  be  described  as  being  a  normal  auricular  wave  in  the  vein. 

The  wave  in  the  ventricular  tracing  which  follows  the  extra  systole 
is  probably  due  to  ventricular  expansion,  and  is  discussed  at  p.  520. 


WITH  EXTRA  SYSTOLES 


519 


Apex 
tracing] 


Venous 
tracings 


Fig.  163. 

This  is  a  portion  of  Tracing  No.  8,  Plate  XI. 

This  tracing,  showing  the  result  of  digitalis,  is  a  good  illustration  of  what 
has  just  been  said  as  to  the  danger  of  accepting  an  interpretation  of  a  tracing 
which  does  not  suffice  to  explain  every  individual  wave  of  the  tracing. 

This  tracing  at  first  seems  to  illustrate  the  passage  of  a  wave  to  and  fro 
between  the  veins  and  the  right  ventricle,  just  as  is  the  case  with  fig.  160  ; 
but  this  interpretation  does  not  apply  to  the  first  rise  in  the  ventricular  tracing 
which  follows  the  extra  systole,  and  more  careful  study  shows  that  this  is 
quite  a  different  tj'pe  of  tracing  from  that  shown  in  fig.  160.  Comparison  of 
the  venous  tracing  with  that  shown  in  fig.  162  and  Tracmg  No.  4,  Plate  IX, 
shows  clearly  that  the  last  wave  of  the  three  small  ones  which  follow  the  normal 
systole  is  really  an  imperfect  true  ventricular  systole  and  that  the  venous  wave 
which  precedes  it  is  the  normal  auricular  wave  occurring  in  its  proper  position 
and  proper  relation  to  the  ventricular  systole.  The  extra  systole — as  might  be 
expected  from  the  effect  of  digitahs — is  much  more  powerful,  and  the  emptying 


520  A  CASE  OF  ARHYTHMIA 

of  the  ventricle  so  sudden,  that  its  recoil  vave  only  shows  on  tlic  base  level  of 
the  tracing,  and  sometimes  it  even  forms  part  of  the  rise  of  the  wave  ■which 
follows  the  cpctra  systole.  Both  these  waves  have  no  corresponding  wave  in 
the  veins,  and  therefore  it  must  be  concluded  that  in  this  instance  the  extra 
systole  does  not  force  blood  into  the  veins  as  is  the  case  in  the  tracing  shown 
in  figs.  IGO,  101. 

The  venous  tracing  is  normal  except  that  the  systohc  rise,  due  to  the  filling 
of  the  first  part  of  the  aorta,  is  later  than  normal,  and  occurs  at  tlie  time  of 
the  second  and  final  aortic  recoil  wave  instead  of  the  first. 

The  pointed  wave  with  a  sudden  drop,  wliicli  follows  the  extra  systole, 
is  not  very  easy  of  explanation  by  means  of  this  tracing  alone.  The 
fact  that  it  coincides  with  the  lowest  point  of  the  venous  tracing,  and  that 
there  is  no  oscillation  in  the  vein  corresponding  either  to  it  or  to  the  extra 
systole,  suggests  that  no  blood  is  forced  into  either  the  auricle  or  the  vein 
by  the  ventricular  activity  which  causes  these  two  waves. 

In  this  instance,  therefore,  the  extra  systole  must  be  forcible  enough  to 
open  the  semilunar  valves  and  empty  the  ventricle  in  the  normal  way.  Un- 
fortunately, in  the  absence  of  a  carotid  tracing  this  point  cannot  be  actually 
proved. 

There  can,  however,  be  little  doubt  that  in  this  case  the  extra  systole 
is  not  only  forcible  enough  to  open  the  semilunar  valves,  but  also  to  cause 
a  true  muscular  expansion  of  the  ventricle,  and  tliis  cxjiansion  movement  is, 
in  all  probability,  the  cause  of  the  rise  wliich  follows  that  due  to  the  extra 
systole. 

Note  that  this  tracing  is  taken  so  far  internal  to  the  main  axis  of  the  heart 
that  the  change  in  volume  which  accomjianies  the  emptying  of  the  ventricles 
causes  a  marked  drop  in  the  cardiogram.  (Compare  this  tracing  with  those  of 
the  type  given  in  Plate  IX,  No.  2,  which  are  taken  over  the  main  axis  of 
the  heart  and  where  the  systolic  rise,  due  to  the  hardening  of  the  cardiac 
muscle,  persists  so  long  as  the  muscle  remains  active.) 

There  is  another  feature  of  this  tracing  which  seems  to  support  what  has 
just  been  said  as  to  most  of  the  blood  being  thrown  forward  through  the  semi- 
lunar valves  by  the  extra  systole  instead  of  back  into  the  veins — namely,  the 
fact  that  the  wave  in  the  vein  caused  by  the  auricular  contraction  is  alwaj^s 
very  small  and  is  sometimes  hardly  visible.  This  points  to  the  fact  that  there 
is  no  abnormal  excess  of  blood  to  be  dealt  with  by  the  right  auricle  such  as 
would  be  certain  to  occur  if  the  extra  systole  did  throw  the  blood  backwards 
through  the  tricuspid  valve  instead  of  forwards.  (Compare  the  size  of  the 
auricular  wave  in  the  vein  in  fig.  160,  where  the  extra  systole  does  result  in 
tricuspid  regurgitation. ) 

The  e^ctreme  smaUness  of  the  wave  due  to  the  auricular  systole  is  also 
to  be  ejcpected  here,  because  of  the  increased  aspiratory  power  which  digitalis 
induces.  The  ventricle  is  so  well  filled  during  its  expansion  phase  that  there 
is  but  little  work  left  for  the  auricular  contraction  to  do.  It  must,  however, 
be  noted,  on  the  other  hand,  that  the  wave  in  the  vein  which  is  synchronous 
W'ith  the  auricular  contraction  is  decidedly  larger  in  those  beats  where  the 
extra  systole  occurs  than  in  the  normal  beats  where  it  docs  not.  Therefore, 
whether  this  particular  wave  be  due  to  the  auricular  systole,  or  to  tricuspid 
regurgitation,  or  (as  is  most  probable)  to  both  combined,  the  increase  in  its 
height  when  an  extra  systole  occurs  shows  that  some  tricuspid  regurgitation 
must — even  in  this  type  of  tracing — result  from  the  extra  systole. 


WITH  EXTRA  SYSTOLES  521 


EXPLANATION  OF  PLATE  XII 

Tliis  figure  shows  a  tracing  taken  over  the  right  auricle  compared  with 
a  ventricular  one,  from  tlie  i)atient  with  extreme  tricusi^id  regurgitation 
whoso  case  is  briefly  referred  to  at  p.  339.  Ventricular  cardiograms  from  the 
patient  are  given  in  Plato  VIII,  Case  V,  which  show  a  very  marked  elevation 
in  tlie  cardiogram  during  the  expansion  phase ;  and  in  tracings  taken  near 
the  sternum  the  higliest  wave  in  the  tracing  occurs  just  after  the  occurrence 
of  the  second  sound. 

In  order  that  the  somewhat  unusual  ventricular  tracing  liere  shown  may 
be  bettor  understood,  a  somewhat  similar  but  more  usual  one  is  given  in  Tracing 
No.  10,  upon  which  was  recorded  the  time  of  occurrence  of  the  first  and  second 
sounds  by  means  of  an  electric  signal. 

This  tracing  shows  that  the  main  rise  is  due  to  the  ventricular  systole ; 
that  the  second  sound  occui's  prior  to  the  occurrence  of  the  second  rise;  and 
that  this  elevation  is  therefore  due  to  the  sudden  enlargement  of  the  ventricle 
as  it  fills  itself  diu-ing  its  expansion  phase. 

The  irregularity  of  the  heart  rhythm  made  it  difficult  to  time  the  first  sound, 
but  the  second  was  timed  witli  fair  accuracy  and  falls  at  or  just  before  the 
highest  point  of  the  second  main  rise. 

The  two  small  waves  which  precede  the  systolic  rise  in  the  tracing  must 
be  of  am-icular  origin  and  jjresumably  represent  the  contraction  of  the  body 
of  the  auricle  followed  by  tliat  of  its  appendix.  (That  they  are  auricular  in 
origin  is  shown  by  the  fact  that  their  distance  from  the  succeeding  systolic 
rise  is  constant,  whilst  that  from  tlie  preceding  one  is  variable.)  On  comparing 
this  tracing  with  the  ventricular  one  shown  in  Tracing  No.  10,  there  is  sufficient 
resemblance  to  make  its  interin'ctation  jiossible. 

Tlie  two  auricular  waves  slu)w  in  both  tracings,  and  tlie  lioUow  after 
the  main  .systolic  rise  occui's  hi  botli,  as  does  the  second  prominence  due  to 
ventricular  expansion. 

In  Tracing  No.  9,  we  can  therefore  say  that  the  first  sound  would  occur 
towards  the  foot  of  the  main  rise,  and  that  the  second  sound  would  occur  just 
at  or  before  the  apex  of  the  second  rise  in  the  ventricular  cardiogram,  and 
the  end  of  the  expansion  phase  would  be,  as  usual,  at  the  foot  of  the  followmg 
fall  in  the  tracing. 

As  regards  the  interpretation  of  the  auricular  part  of  the  tracing  it  is 
necessary  to  jioint  out  that  this  same  type  of  tracing  was  obtainable  all  over 
the  pulsating  area  to  the  right  of  the  sternum  and  with  both  Galabin's  cardio- 
graph and  a  Marey's  drum.  Also  in  some  tracings  the  fall  which  follows  the 
main  rise  did  not,  as  here,  occur  before  the  auricular  contraction,  but  was 
synchronous  with  the  auricular  waves  in  the  apex  cardiogram  and  was  broken 
into  two  portions — one  due  to  the  contraction  of  the  body  of  the  auricle  and 
one  due  to  its  ajjpendix.  These  tracings  have  unfortunately  been  mislaid  and 
cannot  therefore  be  reproduced  here. 

The  phenomenon,  however,  for  which  this  tracing  is  here  reproduced, 
shows  clearly^ — namely,  a  small  pointed  wave  in  the  auricular  tracing  syn- 
chronous with  the  commencement  of  the  ventricular  systole.  The  auricle 
begins  either  to  fill  up,  or  to  contract  again,  at  the  commencement  of  the 
ventricular  contraction,  then  it  contracts  down  again,  causing  a  fall  in  the 
tracing,  and  it  does  not  commence  to  be  over-distended  by  tricuspid 
regurgitation  until  more  than  half  the  systole  is  over. 


522  A  CASE  OF  AKHYTHMIA 

Considering  tliat  in  this  easy  the  luutl  imuniur  duo  to  tlu-  tricuspid  regurgi- 
tation, and  the  distinctly  palpable  thrill  which  accompanied  it,  could  be  clearly 
observed  at  the  very  commencement  of  the  systole  it  is  quite  evident  that  the 
anterior  wall  of  the  auricle  (over  which  the  tracings  were  taken)  must  have 
been  powerfully  contracting  throughout  more  than  one  half  of  the  ventricular 
systole  in  order  to  attempt — albeit  vainly — to  check  the  reflux  through  the 
tricuspid  orifice. 

Note  that  the  main  rise  in  the  aricular  tracing  does  not  always  have  the 
same  relationship  to  the  rise  in  the  ventricular  tracing  which  is  due  to  its 
expansion  phase.  This  is  doubtless  due  to  the  amount  of  tricuspid  regurgitation 
varying  in  the  different  heart  beats  here  recorded. 


SUMMAEY  OF  FACTS  (F.)  AND  THEOEIES  (T.) 
DEDUCIBLE  FEOM  THE  TEACING  SHOWN  IN 
PLATE  X 

(A)     Cause    of    the  Extra    Systole 

1.  (F.)  An  extra  ventricular  systole  is  interpolated  be- 
tween ordinary  cardiac  beats  without  otherwise  altering  the 
cardiac  rhythm. 

2.  (F.)  There  is  no  sign  in  the  venous  tracing  of  any 
auricular  contraction  preceding  or  accompanying  the  com- 
mencement of  the  extra  systole. 

3.  (T.)  Therefore,  the  extra  systole  does  not  appear  to 
be  preceded  by  an  auricular  systole. 

4.  (F.)  Whenever  the  extra  systole  occurs  its  time  relation- 
ship to  the  beat  which  precedes  it  is  always  the  same.  It 
occurs  immediately  after  the  cessation  of  the  cardiac  activity 
due  to  the  preceding  systole.  The  fresh  rise  in  the  cardiogram 
immediately  follows  the  termination  of  the  rise  due  to  the 
preceding  ordinary  systole. 

5.  (F.)  The  extra  systole  occurs  at  the  end  of  the  expan- 
sion phase.  This  is  confirmed  by  the  record  of  the  time  of 
occurrence  of  the  second  sound  upon  the  cardiogram. 

6.  (T.)  The  occurrence  of  the  extra  systole  at  the  exact 
point  when  the  ventricle  has  filled  itself  by  its  own  expansion 
suggests  the  probability  that  this  adventitious  contraction 
is  due  to  the  sudden  stretching  of  the  walls  which  an  over- 
filling of  the  ventricle  would  cause. 

Over- distension  of  the  ventricle  during  the  expansion  phase 
is  evidently  the  cause  of  the  extra  systole  in  this  case. 

7.  (T.)  Two  factors  are  probably  at  work  in  producing 
this  over- distension.  Firstly,  an  over-excitable  heart  giving 
rise  to  an  excessive  aspiratory  force,  and  secondly,  dilated 
auricles  supplying  an  excessive  amount  of  blood  at  the  time 
the  ventricular  suction  occurs. 

523 


524  A  CASE  OF  ARHYTHMIA 

8.  (T.)  If  this  extra  .S3'-stole  be  due  to  the  above  cause, 
drugs  sueh  as  digitalis,  which  mcrease  the  aspiratory  power 
of  the  ventricles,  ought  to  increase  the  arhythrnia,  and  drugs 
such  as  aconite,  which  lessen  the  vigour  of  the  heart's  action, 
ought  to  lessen  the  arhythrnia. 

9.  (F.)  The  arhythrnia  was  markedly  increased  by  digitalis, 
and  markedly  lessened  by  aconite. 

(B).  Facts  and  Theories  Eelating  to  the  Complete- 
ness OF  THE  Extra  Systole,  and  Answering  the 
Question  '  Do  the  Musculi  Papillares  and  the 
Constrictor  Fibres  of  the  Auriculo-Yentricular 
Orifices  Partake  in  the  Ventricular  Contrac- 
tion, so  far  as  the  tracing  shown  in  Plate  X  is 
concerned  ?  ' 

10.  (F.)  The  extra  systole  causes  as  a  rule  no  distinct 
wave  in  the  carotid  arteries,  and  is  always  followed  by  a  very 
distinct  wave  in  the  veins,  which  of  ten.  constitutes  the  highest 
wave  in  the  venous  pulse.  Its  main  effect,  therefore,  in  this 
type  of  tracing  is  to  cause  tricuspid  regurgitation. 

11.  (T.)  Therefore,  the  mitral  and  tricuspid  valves  do  not 
close  properly  (we  must  assumr;  that  the  two  sides  of  the  heart 
act  similarly). 

12.  (T.)  It  is  probable,  as  the  contraction  simply  results 
from  stretching  of  the  muscular  walls  of  the  ventricle  (and  is 
not  due  to  the  normal  spread  of  stimulus  from  the  am*icle), 
that  the  stimulus  to  contract  does  not  involve  both  the  con- 
strictor fibres  of  the  auriculo-ventricular  orifices  and  the 
musculi  papillares  in  due  proportion. 

Work  Done  by  the  Extra  Systole 

13.  (F.)  In  the  tracing  due  to  the  extra  systole  there  is 
a  recoil  wave  similar  to  the  one  in  the  ordinary  sj'stolic  apex 
tracing  (which  is  due  to  the  recoil  of  blood  into  the  ventricle 
from  the  first  part  of  the  aorta  after  the  fh'st  sudden  distension 
of  the  artery). 

14.  (T.)' 

(a)     This  recoil  wave  is  not  due,  in  the  case  of  the  extra 


SUMMARY  525 

systole,  to  distension  of  the  aorta,  because  {¥.),  as  wo 
have  shown,  the  extra  systole  does  not  as  a  rule  cause  any 
wave  in  the  arteries. 
{h)  It  is  not  due  to  the  ineffective  attempt  to  open  the 
semilunar  valves,  because  (F.)  the  tracing  shows  that 
the  recoil  wave  occurs  after  the  ventricle  has  akeady 
considerably  diminished  in  volume  owing  to  the 
expulsion  of  part  of  its  contained  blood.  (It  occurs 
one  third  to  half-way  down  the  wave,  due  to  the  extra 
systole.) 

(c)  It  is  not  duo  to  a  recoil  from  over-distension  of  the 
venous  system  by  the  regurgitating  blood,  because 
(F.)  the  shoulder  of  the  apex  tracing  marking  the  recoil 
wave  distinctly  precedes  the  filling  up  of  the  veins 
(F.).  (The  recoil  wave  in  the  apex  tracing  exactly 
corresponds  to  the  lowest  point  of  the  venous  tracing 
which  precedes  the  rise  just  referred  to.) 

{d)  Therefore,  the  recoil  is  due  to  the  return  of  a  wave 
from  the  auricle  back  to  the  ventricle. 

(G)  Facts  and  Theories  Eegarding  the  Muscular 
Activity  of  the  Auricles  and  Great  Veins  During 
THE  Cardiac  Diastole,  Demonstrating  the  Following 
Proposition 

Stuflij  of  this  case  seems  to  slioio  co7iclusivelij  that  there  is  no 
true  relaxation  or  passivity  of  the  muscular  icalJs  of  the  auricles 
and  great  veiiis,  hut  that  throughout  the  diastole  they  maintain, 
by  tonic  contraction,  a  definite  degree  of  blood  pressure,  and  are 
ready  to  respond  at  once,  by  increased  tonic  activity,  or  by  con- 
tractio7i,  to  any  tendency  to  undue  distension  of  the  auricle  or 
the  veins  by  any  sudden  inrush  of  blood. 

15.  This  proposition  is  supported  by  the  fact  brought 
out  in  paragraph  14.  The  sudden  recoil  of  the  blood  from 
the  auricle  suggests  tonic  activity  on  its  part. 

16.  (T.)  Also  the  fact  that  the  extra  systole  causes  such 
a  marked  wave  in  the  veins  shows  that  either  (1)  the  tonic 
activity  of  the  auricle  is  sufficient  to  resist  the  inrush  of 
the   regurgitating   blood   from   the   ventricle   and   cause    its 


526  A  CASE  OF  ARIIYTHMIA 

diversion  into  the  veins,  or  (2)  that  the  auricle  first  dilates 
under  the  distending  force  of  the  regurgitation,  and  then  by 
a  definite  act  of  contraction  expels  the  blood  into  the  veins. 

In  some  cases  (1)  seems  to  be  the  explanation,  because 
(F.)  the  rise  in  the  vein  exactly  corresponds  to  the  fall  in 
the  apex  tracing,  and  there  is  no  evidence  of  any  increase 
in  the  intraventricular  pressure  such  as  would  be  sure  to 
occur  were  a  definite  contraction  of  the  auricle  to  take  place. 

In  other  instances  (2)  seems  to  be  correct,  for  (F.),  a 
definite  wave,  does  sometimes  appear  in  the  apex  tracing 
(closely  following  the  fall  of  the  wave  after  the  extra 
systole),  such  as  Avould  be  caused  by  an  amicular  con- 
traction, and  this  wave  coincides  with  the  distension  of  the 
vein  just  as  would  be  the  case  were  that  distension  due  to 
an  auricular  systole  aiding  the  regurgitation  from  the  ventricle. 

17.  (F.)  In  some  beats  a  second  rise  occurs  in  the  apex 
tracing  after  the  extra  systole,  due  to  the  return  of  the  blood 
wave  back  from  the  auricle  and  veins  into  the  ventricle  once 
more.  A  sort  of  to-and-fro  oscillation  of  the  blood  between 
the  veins  and  the  ventricle. 

18.  (F.)  In  those  beats,  however,  where  the  presence  of 
the  wave  discussed  in  16  (2)  appears  to  indicate  an  auricular 
contraction,  this  second  oscillation  does  not  occur ;  the  in- 
creased pressure  in  the  vein  (due  to  the  auricular  systole) 
sufficing  to  overpower  the  venous  contraction  and  so  pre- 
vent further  oscillation.  Moreover,  in  these  same  beats  the 
shape  of  the  wave  in  the  veins  as  a  rule  suggests  a  greater 
amount  of  distension  than  in  the  beats  where  there  is  no 
evidence  of  an  auricular  systole.  The  distension  is  more 
prolonged  and  there  is  often  more  or  less  of  a  recoil  wave 
or  shoulder  on  the  wave  in  the  venous  tracing. 

19.  (F.)  "  In  the  beats  where  there  is  no  suggestion  of  an 
extra  auricular  contraction  following  the  extra  systole  there 
is  evidence  {vide  16,  1)  that  the  tonic  activity  of  the  auricle 
alone  causes  the  deflection  of  the  blood  into  the  veins.  In  this 
case  there  is  sometimes  a  second  marked  elevation  in  the  apex 
tracing.  In  such  a  case  the  vein  seems  to  empty  immediately, 
after  the  rise  referred  to,  with  a  suddenness  and  completeness 
suggestive  of  a  contraction  of  its  w^alls,  and  in  such  a  case 


SUMMARY  527 

this  emptying  coincides  with  a  redistension  of  the  ventricle  ; 
the  wave  being  reflected  back  again,  as  it  were,  and  the 
maximal  fall  in  the  vein  corresponds  to  a  point  just  before 
the  maximal  rise  of  the  apex  tracing  {see  third  heat  from 
the  end  of  the  tracing). 

(T.)  Here  again  there  is  fm'ther  evidence  of  tonic  activity 
of  the  auricles,  for  the  rise  in  the  apex  tracing  gradually  attains 
a  maximum.  The  contraction  of  the  great  veins  forces  the 
blood  into  the  tonically  contracted  auricle  and  the  relaxed 
but  nearly  full  ventricle.  The  blood  forced  by  the  venous 
contraction  into  the  auricle  calls  out  a  sHght  muscular 
response,  and  thus  the  maximal  rise  of  the  wave  as  shown 
in  the  ventricle  is  only  attained  just  after  the  emptying  of 
the  veins. 

20.  (F.)  In  addition  to  these  primary  waves  there  are  also 
three  small  oscillations  which  also  show  how  the  blood  between 
the  veins  of  the  neck  and  the  heart  apex  is  practically  a 
continuous  column  under  the  same  pressure. 

(a)  At  the  time  of  the  occurrence  of  the  maximal  wave 
due  to  the  extra  systole,  there  is  sometimes  a  shght 
oscillation,  exactly  synchronous  with  it,  in  the  blood 
in  the  veins  of  the  neck,  then  at  their  emptiest  ((T.) 
owing  to  ventricular  aspiration  of  the  blood  from  the 
auricles  and  veins). 

(b)  In  the  apex  tracing  there  is  often  a  small  wave 
just  after  the  extra  systole,  exactly  synchronous  with 
the  maximal  filling  of  the  vein,  (T.)  as  if  this  distension 
sent  a  shock  down  into  the  ventricle. 

(c)  At  the  time  of  the  maximum  of  the  large  wave  in 
the  apex  tracing,  which  sometimes  follows  the  extra 
systole,  there  is  often  a  small  wave  in  the  nearly  empty 
vein  exactly  synchronous  with  it.  (T.)  Another  recoil 
wave  from  distended  ventricle  to  vein. 


PHYSIOLOGY    OF    THE   AUEICLES   AND    VEINS    AS 
GIVEN  IN  ESSAYS  IX  AND  XVII 

Sequence  of  Events  in  the  Auricles  and  Veins  through- 
out THE  Cardiac  Cycle. — In  view  of  the  facts  brought  out  by 
these  and  similar  observations  upon  the  heart,  it  is  possible  to 
reAvrite  the  sequence  of  changes  which  take  place  in  the  auricle 
and  veins  throughout  the  cardiac  cycle. 

Taking  for  granted  that  the  ventricle  does  fill  itself  by 
its  own  aspiration,  the  following  would  be  the  sequence  of 
events  in  the  auricle. 

The  end  of  the  ventricular  contraction,  just  prior  to  the 
closure  of  the  semilunar  valves,  would,  according  to  this  theory, 
find  the  auricle  at  its  fullest ;  containing  very  nearly  the  full 
charge  of  l)lood  (say,  some  70  c.c.  out  of  the  90  c.c,  which 
represents  the  normal  charge  for  the  ventricle). 

Expansion  phase  of  the  ventricles. — On  the  sudden  ex- 
pansion of  the  ventricles  this  amount  (70  c.c.)  is  aspirated  into 
the  ventricle,  the  ^o  second  during  which  the  expansion  lasts 
sufficing  for  this.  In  the  auricle  this  will  cause  a  sudden  re- 
laxation of  its  walls.  This  sudden  lessening  in  the  tension 
of  its  walls  will,  in  all  probability,  cause  a  slight  muscular 
contraction,  which  will  aid  the  entrance  of  the  last  portion 
of  the  70  c.c.  into  the  ventricle.  The  fact  of  the  auricular 
walls  contracting  down  upon  the  receding  blood,  together  with 
the  tonic  contraction  of  the  auricle  and  great  veins,  wdll  keep 
the  blood  in  the  ventricle  and  prevent  its  return  back  into 
the  auricle  and  the  veins.  The  auriculo-ventricular  valves  may 
also  aid  in  the  retention  in  the  ventricle  of  the  aspirated 
blood.  This  main  emptying  of  the  auricle  does  not  appear 
to  be  accompanied  by  any  powerful  contraction  of  its  walls. 
Such  a  contraction  would  not  be  desirable,  for  it  would  be 
followed  by  an  expansion  phase,  which  would  tend  to  draw 
the  blood  out  of  the  ventricle  back  into  the  auricle. 

Gradual  Filling   of  the   Auricle. — The   auricle    now 

528 


PHYSIOLOGY  OF  THE  AURICLES  AND  VEINS      529 

gradually  fills  with  blood  during  the  remainder  of  the  ven- 
tricular diastole — namely,  its  relaxation  phase — until  the  onset 
of  the  auricular  contraction. 

Degree  of  Fullness  of  the  x\uricle  at  the  Time  of 
ITS  Systole. — Taking  for  granted  that  the  flow  of  blood  into  the 
auricles  is  fairly  regular  tliroughout  the  cardiac  cycle,  it  is  easy 
to  estimate  the  fullness  of  the  auricle  at  the  time  of  its  systole. 
Taking  the  whole  cycle  as  lasting  one  second,  in  a  heart  beating 
sixty  per  minute,  the  whole  of  the  ventricular  relaxation  phase 
lasts  about  0*52  second ;  but  from  this  must  be  deducted  the 
Yo  second  that  the  auricular  systole  lasts.  This  gives  0-42 
second  as  the  time  during  which  the  auricle  is  filling,  and 
therefore  during  this  time  it  will  have  received  42  per  cent,  of 
its  full  charge — namely,  about  38  c.c.  out  of  the  90  c.c.  During 
the  filling,  its  walls  have  been  quietly  distending,  and  its  muscles 
gradually  giving  way  under  the  distensile  force  of  the  entering 
blood. 

Auricular  Systole, — Now  comes  the  main  auricular 
contraction.  The  auricular  systole  must,  according  to  this 
line  of  argument,  be  purely  a  '  nodal  '  phenomenon,  because 
the  fact  that  the  auricle  is  only  partly  full  negatives  the 
possibility  that  mechanical  stimulation  (by  distension)  plays 
any  part  in  it. 

The  auricular  systole  takes  place  in  two  stages.  First  the 
general  wall  of  the  auricle  contracts  so  as  to  raise  the  blood 
pressm'e  within  it.  This  initial  contraction  of  the  auricle 
does  not  always  seem  to  have  the  effect  of  forcing  blood  into 
the  ventricle  or  affecting  its  blood  pressure  sufficiently  to  make 
a  wave  appear  in  the  apex  cardiogram.  Sometimes,  how- 
ever, a  wave  does  show  and  then  it  is  possible  that,  in  these 
cases,  some  blood  is  forced  into  the  ventricle  by  this  first  part 
of  the  auricular  systole.  In  the  venous  tracing,  on  the  other 
hand,  this  initial  contraction  does,  as  a  rule,  show  as  a  distinct 
wave,  and  also  in  tracings  taken  over  the  body  of  the  amicle 
it  is  very  distinct  and,  in  fact,  embraces  nearly  one-half  of  the 
drop  in  the  tracing  due  to  the  auricular  systole. 

The  function  of  this  preliminary  contraction  is  to  prepare 
for  the  more  powerful  contraction  of  the  appendix  by  fixing 
the  walls  of  the  auricle  and  raising  the  pressm'e  within  it. 

2  M 


530      PHYSIOLOGY  OF  THE  AURICLES  AND  VEINS 

Contraction  of  the  Appendix 
Then  follows  the  second  part  of  the  auricular  contraction — 
namely,  the  contraction  of  the  appendix.  The  result  of  this 
is  to  force  a  small  quantity  of  blood  (possibly  some  20  c.c.  or  so) 
into  the  nearly  full  ventricle  (as  described  by  Dr.  Mayo  Collier 
in  1889)  in  order  finally  to  distend  it  and  put  the  auriculo- 
ventricular  valves  on  the  stretch  just  before  they  begin  to  bear 
the  strain  of  the  ventricular  contraction.  The  auricular  con- 
traction has  almost  certainly  another  important  function — 
namely,  to  precipitate  the  contraction  of  the  ventricle  by 
means  of  the  mechanical  stimulation  of  its  muscular  walls 
which  will  result  from  their  sudden  stretchmg.  This  sudden 
stretching  provides  '  the  spark  that  fires  the  powder.'  In 
this  connection  it  is  of  interest  to  remember  that  one  of 
the  principal  results  of  auricular  fibrillation  is  irregularity 
in  the  time  of  occurrence  as  well  as  in  the  strength  of  the 
ventricular  contraction.  This  fairly  forcible  contractile  act 
naturally  makes  a  wave  of  considerable  size  in  the  veins  of 
the  neck,  and  also  causes  a  slight  one  in  the  apex  cardio- 
gram at  the  foot  of  the  systolic  rise. 

Auricular  Aspiration  and  Contraction  of  the  Veins 

This  contraction  of  the  appendix  is,  presumably,  followed 
by  the  usual  elastic  and  muscular  recoil,  and  thereby  develops 
a  certain  amount  of  aspiration,  as  may  be  seen  by  the  venous 
pulse.  As  the  auriculo-ventricular  valves  are  closed,  this 
aspiration  (in  which  the  body  of  the  auricle  may  or  may  not 
take  a  part)  expends  such  force,  as  it  develops,  upon  the  blood 
entering  the  auricle  from  the  veins  and  causes  a  sudden  rehef  of 
pressure  in  them.  As  the  veins  are  at  the  time  distended,  in 
consequence  of  the  reflux  caused  by  the  auricular  systole,  the 
change  is  a  sudden  one,  and  this  sudden  transition  from  full 
distension  to  relaxation  causes  a  marked  drop  in  the  venous 
tracing.  In  the  tracings  here  shown  the  suddenness  and 
depth  of  this  drop  seem  to  show  clearly  that  the  sudden  relaxa- 
tion of  the  stretched  walls  of  the  vein  stimulated  them  to  make 
a  definite  contractile  act.  Such  a  contractile  act  at  this  point 
in  the  cardiac  cycle  will  distinctly  favour  the  filhng  of  the 
auricle  and  prepare  it  for  supplying  the  blood  needed  by  the 
ventricle  during  its  expansion  phase. 


PHYSIOLOGY  OF  THE  AURICLES  AND  VEINS      531 

Ventricular  Systole 

Then  follows  tlio  ventricular  systole.  With  regard  to  its 
origin  this  case  seems  to  show  that  the  stimulus  which  causes  the 
normal  ventricular  systole  is  not  wholly  a  '  nodal  '  one,  but 
that  mechanical  stimulation  by  distension  probably  plays  some 
part. 

Systolic  Wave  in  the  Venous  Pulse 

The  next  phenomenon  to  be  discussed  concerns  the  first 
part  of  the  aorta  and  its  relation  to  the  superior  vena 
cava.  Bearing  in  mind  what  has  ah-eady  been  said  about 
the  degree  of  tone  present  in  the  veins  and  the  fact  that  any 
local  alteration  in  pressure  will  cause  an  immediate  general 
effect,  it  will  be  seen  that  the  sudden  pressure  which  the 
distension  of  the  first  part  of  the  aorta  must  exert  upon  the 
superior  vena  cava  might  be  expected  to  cause  an  impulse  in 
the  veins.  The  tracings  seem  to  prove  that  the  systolic  disten- 
sion of  the  first  part  of  the  aorta  does  cause  the  systolic  rise 
m  the  veins.  The  aortic  recoil  wave  in  the  ventricular  tracing 
has  already  been  referred  to,  and  its  causation  by  the  elastic 
recoil  of  the  first  part  of  the  aorta  after  its  maximal  distension 
has  been  pointed  out. 

Now,  on  comparing  the  systolic  rise  in  the  vem  with  the 
time  of  occurrence  of  this  recoil  wave,  it  is  found  that  they 
are  exactly  synchronous.  This  is  strongly  confirmatory  of 
the  theory  just  advanced  that  this  systolic  wave  in  the  veins 
is  due  to  the  pressure  of  the  distended  first  part  of  the  aorta 
upon  the  superior  vena  cava.  The  alternative  is  that  this 
wave  is  due  either  to  a  slight  amount  of  tricuspid  regurgi- 
tation, or  to  the  pressure  upon  the  column  of  blood  in  the 
veins  by  the  sudden  bulging  of  the  tricuspid  valve  on  the 
commencement  of  the  systole.  Against  these  theories  it  can 
be  pointed  out  that  there  is  no  sign  of  any  filling-up  of  the  vein 
until  after  the  blood  begins  to  enter  the  aorta  and  the  ventricle 
to  diminish  in  volume.  Now  the  valves  will  begin  to  bulge 
towards  the  veins  as  soon  as  the  pressure  begins  to  come  on 
them.  Also  with  regard  to  the  regurgitation  theory,  the 
regurgitation  is  almost  certain  to  continue  throughout  the 
greater  part  of  the  systole,  whereas  the  agency  producing 
this  venous  wave  reaches  its  maximum  at  the  time  of  the 

2  M  2 


532     PHYSIOLOGY  OF  THE  AURICLES  AND  VEINS 

maximum  distension  of  the  liist  part  of  the  aorta  and  then 
rapidly  subsides  towards  the  end  of  the  systole.  This  systolic 
rise  in  the  vein  in  this  case  is  a  very  prominent  feature,  occur- 
ring, as  it  does,  just  when  the  vein  is  at  its  emptiest.  It  here 
forms  the  highest  point  in  the  venous  tracing. 

From  this  the  venous  tracing  falls  again  until  the  shoulder 
occurs  which  marks  the  closure  of  the  semilunar  valves  and  the 
occurrence  of  the  second  sound  of  the  heart.  This  is  again 
followed  by  a  further  fall,  marking  the  emptying  of  the  auricle  by 
the  ventricular  aspiration,  developed  during  its  expansion  phase. 

It  may,  perhaps,  be  thought  that  some  or  even  many  of  the 
deductions  I  have  made  from  these  tracings  rest  upon  an  in- 
secure foundation,  to  say  the  least  of  it.  In  answer  to  this 
criticism,  I  can  only  say  that  the  more  I  study  graphic  records 
of  the  heart,  the  more  reliable  do  I  find  them  to  be.  The  fact 
that  the  principles  of  cardiac  action,  here  advocated,  do  suffice 
to  explain  so  perfectly  the  phenomena  of  cardiac  action,  as 
shown  in  the  venous  and  ventricular  tracings,  is  a  strong  proof 
of  their  accuracy. 


SUMMARY  OF  ARGUMENTS  AND  FACTS 
BROUGHT  FORWARD  IN  THE  PRECED- 
ING PAGES 

Figures  in  black  type  refer  to  imijortant  references. 

Figures  in  small  type  refer  to  ordinary  references. 

Figures  in  parentheses  (8)  refer  to  references  to  clinical  cases. 

A  Summary  and  Index  of  Arguments  and  Facts  brought 
forward  in  connection  with  distensibility  of  the 
Heart  Wall. 

What  Factors  determine  the  Distensibiltty  of  the 
Heart  ? — It  is  evident,  clinically,  that  the  ease  with  which  the 
heart  wall  is  stretched  varies  very  much  according  to  the  age 
and  the  individuality  of  the  patient.  An  amount  of  strain 
that  will  cause  dilatation  of  the  heart  at  one  time  of  life  will 
not  do  so  at  another,  and  the  same  is  true  of  dilTerent 
individuals  at  the  same  time  of  life. 

The  estimation  of  the  amomit  of  distensibility  possessed 
by  any  individual  heart  is  therefore  of  importance  when 
estimating  the  amount  of  its  failure  when  overstrained  in 
any  way,  p.  34. 

This  quality  of  distensibiUty  is  also  of  value  for  classifica- 
tion. 

Upon  what  does  the  heart's  power  of  resisting  dilatation 
depend  ? — p.  6. 

It  may  be  upon  the  muscular  strength  of  its  walls.  It 
may  depend  upon  the  strength  of  the  fibrous  tissues  of  the 
heart  and  pericardium. 

It  is  possible  to  ascertain  the  degree  in  which  each  of  these 
two  factors  is  concerned  in  a  case  of  heart  failure. 

The  muscular  strength  of  the  heart  walls  is  not  the  same 
for  all  parts  of  the  heart. 

533 


534  SUMMAKY 

The  muscular  wall  of  the  left  ventricle  is  evidently  stronger 
than  that  of  the  right. 

The  muscular  wall  of  the  right  ventricle  is  stronger  in 
some  parts  than  in  others,  p.  9. 

So  far  as  the  fibrous  strength  of  the  heart  is  concerned 
there  is  no  anatomical  evidence  that  one  part  is  stronger 
than  another. 

Therefore,  when  the  portions  of  the  heart  wall  which  are 
muscularly  the  w^eakest  are  the  first  to  give  way  in  the  face 
of  overstrain,  it  is  a  justifiable  clinical  deduction  to  say  that 
the  heart  was  evidently  depending  upon  the  strength  of  its 
muscular  wall  for  its  power  of  resisting  dilatation. 

When,  on  the  other  hand,  it  is  found  that  the  parts  of  the 
right  ventricle  wall  which  are  muscularly  the  weakest,  do  not 
dilate  more  readily  than  the  rest  of  the  ventricle  wall,  and  where 
we  find  that  the  left  ventricle,  which  is  muscularly  so  much 
stronger  than  the  right,  dilates  to  the  same  extent  as  the  right 
and  possibly  to  a  greater  extent  (in  the  face  of  overstrain), 
it  is  justifiable  clinicalh^  to  say  that  the  heart  was  depending 
upon  its  fibrous  strength  rather  than  upon  its  muscular  strength 
for  its  power  of  resisting  dilatation. 

This  theory  as  to  the  relative  parts  plaj^ed  by  the  muscular 
and  the  fibrous  strength  of  the  heart  wall  is  confirmed  by  the 
way  in  which  what  we  are  supposing  to  be  the  fibrous  strength 
of  the  heart  wall — as  judged  by  the  type  of  its  dilatation — 
gradually  increases  as  age  advances. 

In  early  hfe  and  adolescence,  when  the  fibrous  tissues  are 
soft  and  immature,  the  heart  dilates  as  if  it  were  dependent 
upon  its  muscular  walls  alone,  pp.  4,  10. 

As  life  -advances,  the  relative  muscular  strength  of  the 
wall  takes  less  and  less  part  in  determining  the  type  of 
dilatation,  just  as  might  be  expected  to  occur  (owing  to 
the  increasing  strength  of  fibrous  tissues)  as  age  advances, 
pp.  5,  11,  31,  76. 

It  can  therefore  be  stated  that : — 

In  adult  life,  clinical  study  of  the  behaviour  of  the  heart 
when  dilating  in  the  face  of  overstrain  shows  that  it  is  dependent 
upon  its  fibrous  strength  rather  than  upon  its  muscular  strength 
for  its  power  of  resisting  dilatation,  p.  10. 


DISTENSIBILITY  OF  THE  HEAET  535 

What  is  the  source  of  its  fibrous  strength  ? 

1.  The  fibrous  tissues  of  the  pericardium  are  generally 
recognised  as  being  of  value  in  aiding  the  heart  to  resist 
dilatation,  p.  5. 

The  fibrous  support  thus  obtained  will  in  part,  but  not 
entirely,  explain  the  phenomena  observable. 

2.  There  must  be  fibrous  elements  in  the  heart  wall  itself 
if  the  phenomena  associated  with  the  lessened  distensibiUty 
that  occurs  in  later  life  are  to  be  explained,  p.  77. 

If,  anatomically,  there  is  insufficient  fibrous  tissue  in  the 
heart  wall  to  account  for  the  loss  of  distensibility  that 
characterises  later  life,  this  loss  of  distensibility  must  be  due 
to  some  change  in  the  muscular  tissue  itself — a  change,  probably 
similar  in  nature  to  that  which,  when  extreme,  is  recognisable 
as  fibroid  degeneration  of  the  heart  muscle,  p.  77. 

This  change — whatever  it  may  actually  be — is  in  this  book 
spoken  of  as  an  '  increasing  rigidity  '  of  the  heart  wall  or  a 
gradually  increasing  firmness  of  '  the  fibrous  elements '  of 
the  heart  wall,  p.  78. 

Variation  in  the  Distensibility  of  the  Heart  according 
TO  THE  Age  of  the  Patient 

I.  Distensibility  of  the  Heart  in  Adolescence. — In 
adolescence  the  fibrous  elements  of  the  heart  wall  and  pericar- 
dium have  little  power  (owing  to  their  softness  and  immaturity) 
of  controlling  the  distensibility  of  the  heart,  which  is  therefore 
liable  to  be  great,  pp.  7,  10. 

Case  illustrating  this,  pp.  (7),  (8). 

The  dependence  of  the  heart  upon  its  muscular  tissue 
alone  for  its  power  of  resisting  dilatation  ensures  the  dilatation 
of  the  thinner  parts  of  the  heart  wall  before  the  thicker  ones, 
pp.  4,  9. 

Consequently,  in  adolescence,  the  right  ventricle  is  more 
distensible  than  the  left. 

Therefore,  in  overstrain  the  right  ventricle  will  be  the 
first  to  give  way,  and  the  left  ventricle,  will  be  thus  protected 
by  the  weakness  of  the  right,  pp.  5,  11. 

Heart  failure  will,  therefore,  show  first  on  the  right  side 


536  SUMMARY 

whether  primarily  involving  the  left  or  the  right  ventricle, 
p.  2. 

Also  in  adolescence,  the  thinner  parts  of  the  right  ventricle 
wall  will  yield  before  the  stronger  parts  and  thus  produce  a 
characteristic  type  of  dilatation,  p.  9. 

In  adolescence,  the  thinness  of  the  upper  part  of  the 
anterior  wall  near  the  pulmonary  valves  causes  this  part  of 
the  wall  to  dilate,  in  face  of  overstrain,  before  the  rest,  pp.  4, 
211. 

This  dilatation  of  the  right  ventricle  upwards  and  to  the 
left  may  be  called  the  adolescent  type  of  dilatation,  p.  9. 

The  circumstances  under  which  this  adolescent  type  of 
distensibilit}^  may  occur  are  : — 

1.  In  adolescence  owdng  to  immaturity  of  fibrous  tissues. 

2.  Personal  idiosyncrasy.  In  some  elderly  persons  the 
distensibility  of  the  heart  resembles  that  of  an  adolescent, 
pp.  32,  33,  82,  (83),  (85). 

3.  The  fibrous  tissues  may  be  softened  by  disease,  and 
thus  lose  some  of  their  resisting  power — notably  so  in  the  case 
of  acute  rheumatism,  p.  11,  343. 

II.  Distensibility  or  the  Heaet  in  Adult  Life. — The 
gradual  consolidation  and  hardening  of  the  fibrous  tissues 
which  accompanies  the  passing  of  adolescence  into  adult 
life  causes  a  gradual  change  in  the  distensibility  of  the  heart, 
pp.  5,  11,  72,  79. 

Tbe  distensibihty  of  the  two  ventricles  gradually  becomes 
more  nearly  equal,  and  consequently  the  relative  frequence 
of  dilatation  of  the  left  ventricle  increases,  5,  31,  309. 

The  special  distensibility  of  the  thin  part  of  the  anterior 
wall  of  the  right  ventricle  is  gradually  lost,  and  the  adult 
type  of  dilatation  gradually  replaces  the  adolescent  as  age 
advances,  pp.  11,  31.  33. 

III.  Distensibility  of  the  Heart  in  Later  Life.  — 
The  lessening  of  distensibility,  which  characterised  the  change 
from  adolescent  to  adult  life,  is  still  more  marked  as  age  ad- 
vances ;  and  in  later  life  the  heart,  as  a  rule,  loses  a  good  deal 
of  its  distensibility  and  becomes  what  may  for  convenience 
be  called  *  relatively  rigid,'  pp.  73,  76,  79. 


DISTENSIBILITY  OF  THE  HEART  537 

Dilatation,  when  it  occurs,  is  usually  of  the  adult  type, 
pp.  73,  85. 

Exceptionally,  as  a  result  of  personal  idiosyncrasy,  dilata- 
tion 7nay  he  of  the  adolescent  type,  pp.  82,  (83),  (85). 

Sometimes  the  increase  in  rigidity  of  the  fibrous  elements 
may  be  so  great  that  the  ordinary  force  of  the  ventricular 
contraction  is  insufficient  to  cause  dilatation  of  the  heart  walls. 

A  clinical  group  must  therefore  be  recognised  where  heart 
failure  without  enlargement  of  the  heart  occurs  in  hearts  of 
good  muscular  strength,  but  whose  walls  are  abnormally  rigid, 
pp.  73,  86,  (87),  (89). 

The  lessened  distensibility  has  the  effect  of  lessening  the 
frequency  with  which  dilatation  of  the  heart  occurs  in  cases 
of  overstrain  of  all  sorts  in  later  life,  pp.  73,  79,  85. 

It  also  lessens  the  amount  of  dilatation  that  will  result 
from  any  definite  degree  of  overstrain— in  comparison  with 
the  more  distensible  heart  of  a  j^ounger  individual  (pp.  73,  87). 

The  estimation  of  the  degree  of  rigidity  of  the  heart  wall 
is  therefore  of  great  importance  in  cardiac  diagnosis  in  later 
hfe,  pp.  34,  247. 

Distensibility   in   Eelation  to  Heart   Failure  \vithout 
Enlargement 

The  distensibilit}^  of  the  heart  must  also  be  considered 
in  relation  to  the  cases  of  heart  failure  without  dilatation 
which  occur  where  there  is  great  myocardial  wealmess. 

The  clinical  phenomena  observable  in  cases  of  myocardial 
weakness  are  very  different  in  early  life  (when  the  heart  walls 
are  distensible)  from  what  they  are  in  later  life  when  they 
are  more  rigid. 

In  the  first  two  or  three  decades  of  life  a  diminution  in 
the  size  of  the  cardiac  dullness  and  in  the  distinctness  of  its 
impulse,  together  with  evidences  of  a  diminution  in  the  A^olume 
of  the  blood  in  circulation,  are  observable,  pp.  50,  54,  186. 

The  extent  of  these  changes  is  proportional  to  the  degree 
of  cardiac  weakness  present,  and  in  extreme  cases  there  may 
be  not  only  complete  absence  of  all  cardiac  impulse,  but  also 
complete  absence  of  all  signs  of  cardiac  dullness  as  well.  The 
full  gastric  resonance  will,  in  such  a  case,  come  up  to  meet  the  full 


538  SUMMARY 

lung  resonance  somewhere  about  the  fourth  left  interspace, 
giving  evidence  of  great  diminution  in  the  volume  of  the  intra- 
thoracic contents.  The  deficiency  must  be  due  to  a  diminu- 
tion in  the  amount  of  blood  in  the  lungs,  heart",  &c.,  pp.  50, 
56,  (119),  179. 

The  causal  relationship  between  the  heart  weakness  and 
the  clinical  evidences  of  its  smallness  is  confirmed  by  the 
gradual  return  of  the  heart  to  its  normal  size  as  strength 
returns,  pp.  63,  64,  (68),  (196). 

The  clinical  phenomena  here  spoken  of  caimot  be  due 
to  a  diminution  in  the  actual  bulk  of  the  cardiac  tissue,  but 
only  to  the  degree  to  which  the  heart  is  filled.  The  term 
'  smallness  '  only  refers  to  the  heart  when  full.  The  heart 
when  at  its  emptiest  must  be  the  same  size  as  normal.  As, 
however,  the  heart  does  not  remain  empty  for  much  more 
than  -j-(j  of  a  second  (vide  p.  386),  the  heart  which  we  percuss 
clinically  is  the  full  heart. 

In  the  distensible  heart  of  adolescence,  we  are  justified 
in  saying  that  the  heart  diminishes  in  size  proportionally  to 
the  amount  of  myocardial  weakness  present,  p.  81. 

In  the  less  distensible  heart  of  adult  life,  the  diminution 
in  the  size  of  the  heart  in  cases  of  myocardial  weakness  is 
less  extreme  and  may  be  comparatively  slight,  pp.  81,  (158). 

In  adult  and  later  life,  valuable  evidence  of  dangerous 
myocardial  weakness  may  be  given  by  the  failure  of  a  heart 
to  dilate  under  circumstances  which,  considering  its  degree  of 
distensibility,  ought  to  have  caused  dilatation,  pp.  (64),  71. 

Cases  of  pneumonia  where  the  absence  of  cardiac  dilata- 
tion showed  dangerous  myocardial  weakness,  pp.  (97),  (105). 

In  the  relatively  rigid  heart  of  later  life,  there  is  often 
little  or  no  certain  evidence  of  any  diminution  in  the  size 
of  the  heart  in  cases  of  extreme  weakness.  In  such  cases 
it  is  justifiable  to  deduce  that  the  degree  of  rigidity  present 
prevents  any  lessening  in  the  size  of  the  very  weak  heart 
just  as  the  presence  of  rigidity  in  a  fairly  strong  heart  may 
prevent  the  occurrence  of  dilatation  when  heart  failure  from 
overstrain  occurs,  pp.  74,  79,  91. 

Therefore,  in  the  more  rigid  heart  of  later  life,  signs   of 


BISTENSIBILITY  OF  THE  HEART  539 

myocardial  weakness  must  be  looked  for  in  connection  with  com- 
pensatory diminution  in  the  amount  of  blood  in  circulation  rather 
than  in  connection  with  changes  in  the  heart  itself,  pp.  57,  94. 

Clinical  Estimation  of  the  Distensibility  of  the 
Heart. — It  is  evident  that  we  cannot  estimate  correctly  the 
clinical  significance  of  the  lyresence  or  of  the  absence  of  altera- 
tions in  the  size  of  the  heart  in  cases  of  heart  failure,  unless 
some  estimate  can  at  the  same  time  be  made  of  the  amount 
of  distensibility  of  the  heart  wall,  p.  34. 

In  Early  Adolescence,  the  estimation  of  the  heart's 
distensibility  is  easy,  owing  to  the  ready  response  of  the 
heart  wall,  either  by  enlargement  or  by  diminution  in  size, 
to  alterations  in  the  mode  of  action  of  the  heart,  p.  10. 

In  a  moderately  strong  heart,  the  distensibility  is  shown 
by  the  readiness  with  which  the  heart  dilates  and  by  the 
extent  of  the  dilatation  when  overstrained,  and  in  a  very 
weak  heart  by  the  readiness  with  which  the  cardiac  dullness 
diminishes  in  size  and  by  the  extent  of  that  diminution, 
pp.  10,  52,  54. 

In  Late  Adolescence,  a  slight  lessening  in  the  heart's 
distensibility  will  be  shown  by  the  occurrence  of  some  dilatation 
of  the  right  ventricle  towards  the  right  (in  moderate  degrees 
of  overstrain),  i.e.  by  a  tendency  towards  the  adult  type  of 
dilatation,  p.  33. 

In  Adult  and  Later  Life — I.  In  hearts  of  good  or 
moderate  strength  (as  judged  hj  the  cardiac  sounds  and 
impulse,  and  the  jugular  bulb  pulsation,  &c.). 

1.  Considerable  distensibility  will  be  shown  by  the  occur- 
rence (when  the  heart  is  overstrained)  of  a  combination  of  the 
the  adolescent  and  the  adult  types  of  dilatation  of  the  right 
ventricle. 

A  greater  preponderance  of  the  adolescent  type  will  show  a 
higher  degree  of  distensibility,  and  vice  versa,  pp.  11,  33. 

A  preponderance  of  right-sided  dilatation,  as  compared  with 
left-sided,  will  also  show  a  high  degree  of  distensibility,  p.  11. 

2.  A  less  degree  of  distensibility  will  be  shown  when  the 
adult  type  alone  occurs  ;  and  the  more  dilatation  of  the  left 
ventricle  in  overstrain  preponderates  over  that  of  the  right  the 
less  must  the  heart's  distensibilit}^  be,  p.  11. 


540  SUMMARY 

Also  the  less  the  amount  of  dilatation  that  occurs  with  any- 
definite  degree  of  overstrain  the  greater  must  the  relative 
'  rigidity  '  of  the  heart  be,  p.  86. 

8.  If  cardiac  failure  be  unaccompanied  by  dilatation  it 
shows  a  great  lessening  in  the  distensibility  of  the  heart  (i.e. 
a  considerable  amount  of  '  rigidity  ').  The  degree  of  rigidity  is 
measured  by  the  amount  of  cardiac  overaction  observable, 
pp.  86,  148. 

(It  can  safely  be  asserted  that  a  heart  which  shows  *  failure 
without  enlargement '  in  spite  of  a  considerable  amount  of  over- 
action  is  giving  more  evidence  of  rigidity  of  its  walls  than  one 
which  shows  '  failure  without  enlargement '  in  combination 
with  a  less  amount  of  overaction,  p.  8.) 

Abnormal  rigidity  of  the  heart  wall  can  be  diagnosed  when 
the  heart  fails  to  dilate  under  circumstances  that  might 
reasonably  be  expected  to  lead  to  dilatation,  pp.  73,  (87), 
(89). 

Evidences  of  increased  right  ventricle  activity  are  of  value 
in  estimating  the  amount  of  cardiac  rigidity  in  later  life, 
p.  86. 

Diagnostic  value  of  seeing  the  relationship  of  the  strength 
of  the  venous  pulse  in  the  jugular  bulb  to  the  amount  of 
dilatation,  pp.  (87),  97,  137. 

II.  In  hearts  of  considerable  muscular  weakness  (as 
judged  by  the  cardiac  sounds  and  impulse  and  the  evidences 
of  compensatory  reduction  in  the  volume  of  blood  in 
circulation). 

1.  The  presence  of  some  degree  of  '  rigidity  '  (i.e.  loss  of 
distensibility)  will  be  shown  by  the  fact  that  the  diminution 
in  the  size  of  the  cardiac  dulhiess  is  not  so  great  as  would  be 
noticeable  in  the  heart  of  an  adolescent  with  the  same  amount 
of  cardiac  weakness,  p.  96. 

2.  A  higher  degree  of  '  rigidity  '  will  be  shown  by 
the  fact  that  there  is  no  reduction  at  all  in  the  size  of  the 
heart. 

The  greater  the  degree  of  weakness  which  is  present  the 
stronger  will  the  evidence  of  '  rigidity'  be,  pp.  91.  112,  150. 

3.  Where  a  heart  shows  no  diminution  in  its  size  in  spite  of 
considerable  weakness  and  it  is  therefore  difficult  to  estimate  the 


DLSTENSIBILITY  OF  THE  HEART  541 

actual  amount  of  its  distensibility,  it  it;  nevertheless  sometimes 
possible  to  do  so,  o)i  its  recovery,  by  noting  the  occurrence  of 
'  dilatation  as  a  sign  of  returning  strength.'  For  this  purpose 
the  size  of  the  right  ventricle,  as  shown  by  the  amount  of 
dulhiess  in  the  third  left  interspace,  and  in  the  fourth  and  fifth 
left  and  right  interspaces  near  the  sternum,  must  be  very 
carefully  watched,  p.  63. 

4.  Often  in  later  life  it  is  not  possible  (when  the  heart  is 
relatively  rigid)  to  estimate  with  any  certainty  the  degree  of 
muscular  weakness  that  is  present  (owmg  to  the  uncertainty  as 
to  the  indications  given  by  the  pulse  and  the  blood  pressure, 
if  normal  or  higher  than  normal,  p.  143,  and  to  the  inter- 
ference, due  to  tissue  rigidity,  with  the  indications  that  would 
be  given  otherwise  by  compensatory  lessening  of  the  blood 
volume,  p.  72. 

In  such  a  case  no  estimate  of  the  rigidity  may  be  possible, 
p.  148. 

5.  The  presence  of  sympoms  of  heart  weakness  unaccom- 
panied by  diminution  in  the  size  of  the  heart  and  without 
evidence  of  a  compensatory  reduction  in  the  blood  volume 
points  to  the  presence  of  a  dangerous  amount  of  rigidity  of 
the  heart  walls. 

Diagnostic  points  in  very  weak  hearts,  p.  147. 
Very  weak    heart   showing    distensibility    in    later     life, 
pp.  (157),  (159). 

Post-mortem  estimate  of  the  distensibihty  of  the  heart. — 
This  is  possible  in  early  life,  to  some  extent.  In  later  life 
the  changes  due  to  rigor  mortis  would  probably  interfere 
with  any  useful  estimate  being  made,  p.  81. 


542  SUMMARY 

A  Summary  and  Index  of  Arguments  and  Facts  brought 

FORWARD    IN     CONNECTION     WITH    HeART    FaILURE    WITH 

Enlargement 

Factors  which  Determine  the  Type  and   the  Amount 
OF  Cardiac  Dilatation 

The  question  of  dilatation  of  the  heart  is  a  simi^le  one. 

If  the  intraventricular  pressure  developed  by  the  muscular 
wall  exceeds  the  resisting  power  of  the  weakest  part  of  the 
wall,  that  part  will  be  stretched  and  heart  failure  with  dilatation 
will  result,  pp.  6,  9,  31. 

If  intraventricular  pressure,  in  excess  of  the  resisting 
power  of  the  ventricle  walls,  cannot  be  developed,  no  dilatation 
of  the  ventricles  can  occur  and  heart  failure  ivWioiit  enlargement, 
will  result,  pp.  6,  54,  86,  91. 

In  other  words,  dilatation  results  when  the  force  developed 
by  the  stronger  portions  of  the  ventricle  wall  causes  over- 
distension of  the  weaker  parts,  pp.  6,  31,  211. 

Which  part  of  the  heart  wall  is  the  weakest  ? 

For  its  power  of  resisting  dilatation  the  heart  depends  on 
two  factors  : — ■ 

1.  The  resisting  power  of  the  fibrous  elements  of  its  walls 
— especially  the  pericardium,  both  visceral  and  parietal, 
pp.  5,  31. 

2.  The  tonic  strength  of  its  muscular  walls,  pp.  4,  9. 

The  fibrous  tissues  gain  in  strength  and  resisting  power 
with  maturity,  and  upon  them  the  heart  mainly  depends  in 
adult  life  for  its  power  of  resisting  dilatation,  pp.  5,  11,  31, 
33,  76. 

The  fibrous  tissues  continue  to  increase  in  strength  and 
resisting  power,  as  a  rule,  as  age  advances. 

The  amount  and  the  type  of  cardiac  dilatation  may  therefore 
be  expected  gradually  to  change  as  age  advances. 

The  heart  in  later  life  has  more  '  mechanical '  (as  distinct 
from  muscular)  resisting  power.  It  has  less  '  distensibility  ' 
and  more  '  rigidity,'  pp.  73,  76. 

Dilatation  is  less  frequently  a  result  of  overstrain  than 
was  the  case  earlier  in  life,  pp.  31,  71,  73,  76,  87. 


HEART  FAILURE  WITH  ENLARGEMENT  543 


Various  Types  of  Dilatation 

1.  In  Adult  Life,  when  the  fibrous  tissues  have  good 
resisting  i)ower,  in  the  case  of  both  right  and  left  ventricles, 
the  apical  portion  seems  cluiically  somewhat  stronger  than 
the  basal  part,  and  therefore  the  relative  muscular  thimiess 
of  this  latter  portion  must  take  some  share  in  determining 
where  dilatation  will  occur,  p.  31. 

Dilatation,  when  it  occurs,  mainly  involves  the  part  of  the 
ventricle  wall  which  is  adjacent  to  the  auriclo-ventricular 
valve,  pp.  5,  10. 

In  the  case  of  the  left  ventricle  this  causes  a  widening 
of  the  base  of  the  ventricle  towards  the  left,  and  in  the  case 
of  the  right  ventricle  a  widening  towards  the  right,  pp.  47, 40. 

This  constitutes  what  may  be  called  the  adult  type  of 
dilatation,  pp.  ii,  31,  &c. 

The  thinness  of  this  basal  portion  has  a  most  important 
action  in  safeguarding  the  ventricle. 

Its  dilatation,  when  it  reaches  a  certam  point,  so  affects 
the  auriculo -ventricular  orifice  as  to  cause  incompetence 
of  the  valve  and  escape  of  some  of  the  ventricular  contents 
into  the  auricle,  p.  32. 

Were  it  not  for  this  well-known  safety-valve  action,  dila- 
tation of  the  ventricle,  having  once  started,  would  rapidly 
increase  till  the  walls  either  gave  way  or  became  too  thin 
to  maintain  adequate  blood  pressure,  p.  32. 

In  Later  Life,  when  the  fibrous  tissues  are  more  resistant 
still,  there  may  be  so  much  gain  in  the  resisting  power  of 
the  fibrous  elements  that  these  thinner  portions  of  the  heart 
walls  lose  their  relative  distensibihty.  When  this  takes 
place  no  dilatation  of  the  ventricle  can  occur  (owing  to  the 
inadequacy  of  such  force  as  it  can  develop),  and  then  any 
enlargement  would  be  confined  to  the  auricles  and  great 
veins,  p.  86. 

2.  Adolescent  Type  op  Dilatation. — In  the  early 
decades  of  life,  on  the  other  hand,  when,  owing  to  immaturity 
or  other  cause,  the  fibrous  elements  of  the  heart  wall  and 
pericardium  have  little  or  no  resisting  power,  the  heart  will 


544  SUMMARY 

dilate  as  if  it  were  dependent  upon  the  strength  of  its  muscular 
walls  alone,  pp.  4,  9. 

Under  these  circumstances  in  the  case  of  the  left 
VENTRICLE,  there  is  no  evidence  that  the  type  of  dilatation 
is  materially  different  from  that  occurring  when  the  fibrous 
elements  have  good  resisting  power. 

In  the  case  of  the  right  ventricle,  however,  there  is  a 
well-marked  departure  from  the  type  just  described ;  for  certain 
parts  of  the  ventricle  wall  are  decidedly  weaker  muscularly 
than  the  rest,  and  these  are  the  first  to  give  way  in  the  face 
of  any  abnormal  strain  or  vfhen  for  any  cause  the  muscle  is 
abnormally  weak,  pp.  4,  9. 

The  weakest  parts  are  the  conus  arteriosus  and  the  adjacent 
part  of  the  anterior  wall  of  the  ventricle,  p.  9. 

The  strongest  parts  are  the  interventricular  septum  and 
the  apical  portion  of  the  ventricle,  in  consequence  of  its 
muscular  bands. 

Intermediate  in  strength  is  the  part  adjacent  to  the 
auriculo-ventricular  groove  and  the  remainder  of  the  anterior 
wall. 

Also,  in  consequence  of  the  relative  nmscular  weakness 
of  the  right  ventricle  as  compared  with  the  left,  dilatation  is, 
usually,  confined  to  the  right  ventricle  alone,  unless  the  heart 
is  severely  overstrained,  pp.  5,  46,   308. 

When  may  this  type  of  dilatation  be  expected  to  occur  ? 
In  early  life,  up  to  and  including  adolescence,  the  softness 
and  immaturity  of  the  fibrous  elements  wiU  so  greatly  lessen 
their  resisting  power  as  to  make  the  heart  dependent,  almost 
entirely,  upon  its  muscular  strength  for  its  power  of  resisting 
dilatation.  In  adolescence,  therefore,  the  thin  part  of  the 
anterior  wall  which  is  adjacent  to  the  puhnonary  valves  will 
be  the  first  to  yield  in  the  face  of  overstrain,  and  the  resultmg 
type  of  dilatation  may  well  be  called  the  adolescent  type, 
pp.  5,  9,  330,  &c. 

Adult  and  adolescent  types  of  dilatation  compared,  pp.  5, 
33,  330. 

The  adolescent  type  of  dilatation  will  also  occur  apart 
from  '  absolute '  overstrain,  whenever  the  muscular  strength  of 
the  wall  is  lessened  from  malnutrition  or  other  cause.     These 


HEART  FAILURE  WITH  ENLARGEMENT  515 

may  bo  called  cases  of  '  relative  '  overstrain.  For  instance, 
in  cases  of  simple  anaemia,  where  there  is  no  overaction  of 
the  right  ventricle,  or  where  the  heart  is  recovering  from 
myocardial  weakness,  pp.  63,  (2<)()),  (304). 

The  adolescent  type  of  dilatation  will  also  be  fomid  in 
adult  life  wherever  the  resisting  power  of  the  fibrous  elements 
of  the  heart  wall  is  less  than  normal  in  consequence  of  disease 
— such  as  acute  rheumatism— or  in  consequence  of  personal 
idiosyncrasy,  pp.  ii,  82,  343. 

Adolescent  type  of  dilatation  in  later  hfe  after  the  age 
of  fifty,  pp.  (83),  (85). 

The  amount  and  the  type  of  dilatation  found  as 
age  advances  ^nll  be  determined  by  the  degree  of  matm'ity 
attained  by  the  fibrous  tissues,  and  the  adolescent  type  will 
year  by  year  gi-adually  change  uato  the  adult  type,  pp.  5,33. 

3.  Intermediate  Types  of  Dilatation.  —  The  above 
two  types  of  dilatation  only  occur,  as  a  rule,  in  late  adult 
hfe  and  in  early  adolescence,  respectively.  In  the  intermediate 
period  of  hfe,  intermediate  types  usually  occur,  p.  33. 

Apportionment  of  Strain  between  the  Eight  and  Left 

\'entricles 

In  the  first  place  the  word  '  strain  '  needs  definition  ;  for  a 
normally  strong  heart  may  be  overstrained  through  excess  of 
work — this  is  a  condition  of  '  absolute  overstrain.'  Or  the 
overstrain  maj^  result  fi'om  the  heart  being  too  weak  to  do 
an  amount  of  work  that  does  not  exceed  its  normal  limits 
— a  condition  of  '  relative  overstrain,'  pp.  310,  342. 

Conditions  causing  Overstrain 

1.  Ordinary  physical  exertion,  pp.  (310),  (316). 

2.  Anything  interfering  with  the  pulmonary  circulation — 
such  as  pneumonia,  or  the  simple  anaemia  of  adolescence,  pp.  245, 
343,  (360). 

3.  The  extra  work  thrown  upon  the  right  heart  by  valvular 
disease  of  the  left  ventricle,  p.  343. 

Amongst  the  causes  of  relative  overstrain  all  causes  of 
cardiac  weakness  would  have  to  be  mentioned,  and  promuiently 

2n 


546  SUMMARY 

amongst  them — so  far  as  clinical  importance  is  concerned — the 
weakening  of  the  heart  muscle  due  to  such  infective  conditions 
as  influenza  and  diphtheria,  and  the  softening  and  weakening 
of  the  heart  which  results  from  rheumatism,  pp.  11,  343. 

As  regards  the  apportionment  of  strain  between  the  two 
ventricles,  the  last  two  causes  of  absolute  overstrain  involve 
the  right  ventricle  only. 

As  regards  the  strain  of  physical  over-exertion. 

In  adolescence  the  weakness  of  the  right  ventricle  so  protect  ?. 
the  left  that  it  is  not  easy  to  say  that  any  particular  type  of 
strain  involves  one  ventricle  more  than  the  other,  pp.  46,  309. 

Under  adolescent  conditions,  therefore,  signs  of  overstrain 
must  be  looked  for  as  a  rule  m  the  right  ventricle,  even  though 
the  strain  be  more  likely  to  involve  the  left  side,  pp.  11,  308, 

Under  adult  conditions  the  resisting  power  of  the  two 
ventricles  being  more  nearly  equal,  overstrain  usually  involves 
the  left  ventricle  as  well  as  the  right,  pp.  308,  316. 

Careful  observation  as  to  the  effects  of  different  types 
of  over-exertion  might  show  that  some  kinds  involve  one 
ventrica,l  more  than  the  other,  p.  310. 

But  the  inaccessibility  of  the  left  ventricle  would  prevent 
slight  signs  of  failure  being  noticeable,  pp.  2,  47. 

Also  the  structural  arrangements  of  the  left  ventricle 
ensure  that  any  ineffective  action  on  its  part  immediately 
causes  embarrassment  of  the  right,  and  so  tends  to  divide 
the  strain  between  the  two  sides  of  the  heart,  p.  2. 

Pathological  Aspects  of  Dilatation  of  the  Eight 
Ventricle  in  i\.D0LESCENCE  and  Early  Adult  Life, 
p.  247 

Enlargement  up  and  to  the  left,  pp.  233,  247. 

Change  in  level  of  pulmonary  valves  caused  by  upward 
dilatation  ;  sometimes  under  first  rib,  pp.  (233),  (251). 

1.  Changes  in  pulmonary  artery,  p.  251. 

It  is  shortened,  thus  causing  relaxation  of  its  elastic  walls, 
pp.  (233),  252,  262. 

It  is  often  displaced  as  much  as  one  inch  to  the  left  of 
its  normal  position,  vide  figs.  60,  61,  p.  248. 


HEART  FAILURE  WITH  ENLARGEMENT  547 

It  is  brought  nearer  to  the  anterior  chest  wall. 

Its  direction  in  relation  to  the  axis  of  the  right  ventricle 
is  altered,  pp.  252,  336. 

It  is  liable  to  undergo  temporary  aneurysmal  dilatation 
under  normal  or  increased  systolic  blood  pressure,  p.  253. 

Its  relationship  to  the  aortic  arch  is  altered,  pp.  215,  259. 

Enlargement  to  the  right  is  not  present  in  heart  failure 
of  adolescence  unless  dilatation  be  extreme,  pp.  238,  354. 

Position  of  the  right  auriculo-ventricular  groove  in 
adolescent  dilatation,  and  in  dilatation  towards  the  right, 
pp.  41,  (236). 

Dilatation  of  the  right  auricle  does  not  usually  cause 
dullness  or  pulsation  observable  clinically,  p.  41. 

A  Summary  and  Index  of  Arguments  and  Facts  brought 

FORWARD    IN    CONNECTION  WITH   THE    ClINICAL    ASPECTS 

OF  Heart  Failure  with  Enlargement 

When  the  Heart  is  Distensible  or  Moderately 
Distensible. — Early  signs  of  heart  failure  show  first  in  the 
right  ventricle  for  anatomical  and  physiological  reasons,  p.  2. 

In  the  distensible  heart  of  adolescence  the  relative  weakness 
of  the  right  side  so  saves  the  left,  that  evidences  of  heart  failure, 
unless  it  be  extreme,  are  practically  limited  to  the  right 
ventricle,  pp.  11,  46,  309. 

In  the  extreme  heart  failure,  due  to  valvular  disease  of  the 
left  ventricle,  phenomena,  usually  associated  with  the  adult 
type  of  dilatation,  may  be  superadded  to  those  characteristic 
of  heart  failure  in  adolescence,  pp.  30,  (339). 

Adolescent  or  Upward   Type   of   Dilatation  of  the 
Eight  Ventricle 

Symptoms,  pp.  12,  342. 

Breathlessness.     Belief  by  a  '  deep  breath,'  pp.  14,  22. 
Pain  and  tenderness.     Globus  hystericus,  pp.  14,  212,  342. 
Physical  signs,  pp.  17,  330. 

Veins  of  neck  ;  fullness  and  false  pulsation,  pp.  14.  137,  332. 
Inspection  of  the  heart,  pp.  17,  331. 

Increased  cardiac  pulsation  in  third  and  second  inter- 
spaces, pp.  17,  331. 


548  SUMMARY 

Character  of  tlio  impulse  on  inspeciion,  pp.  17,  331. 

Greater  at  end  of  inspiration,  pp.  18,  232. 

Passage  of  wave  of  contraction  down  and  out,  p.  18. 

Palpation  of  the  heart  in  the  adolescent  type  of  dilatation. 

Situation  of  apex,  often  in  fourth  interspace,  pp.  19,  234, 
237,  332,  349. 

Great  increase  in  area  of  cardiac  pulsation  in  well-marked 
case,  p.  (306). 

Diagnostic  value  of  pulsation  felt  in  the  third  left  inter- 
space in  and  external  to  the  nipple  line,  p.  19. 

Shock  due  to  the  closure  of  the  pulmonary  valves,  often 
felt  in  second  interspace  and  sometimes  some  distance  from 
the  sternum  when  overstrain  is  severe,  as  in  the  heart  failure 
of  anaemia,  pp.  232,  (286),  332. 

Presence  of  a  systoHc  thrill  over  pulmonary  artery  in 
anaemia,  pp.  19,  255,  332. 

Thrill  conducted  to  arteries  of  neck,  especially  left  carotid, 
pp.  216,  259,  (291). 

No  increase  to  right  of  sternum  in  adolescent  type  of 
dilatation,  pp.  (286),  238,  354. 

Upward  dilatation  of  ventricle  implies  the  absence  of 
tricuspid  regurgitation  unless  heart  failure  be  extreme,  pp.  211, 
239,  269. 

Percussion  of  the  heart  in  adolescent  type  of  dilatation, 
pp.  25,  332. 

Method  of  percussion.  Value  of  both  strong  and  hght 
percussion,  p.  20. 

Increase  of  cardiac  dullness  upwards  and  to  the  left,  pp.  25, 
211,  228. 

Usually  both  upwards  and  outwards,  p.  289. 

Sometmies  mainly  upwards,  p.  290. 

Sometimes  involves  only  the  conus  arteriosus,  pp.  292, 
(293),  (294). 

Extra  strain  on  the  conus  arteriosus,  p.  10. 

Dilatation  of  conus  alone  is  a  sign  of  myocardial  weakness, 
p.  293. 

Sometimes  dilatation  is  mainly  outwards  to  the  left,  p.  298.  ^ 

Diversity  of  type  in  the  overstram  in  anaemia,  p.  289. 


HEART  FAILURE  WITH  ENLARC4EMENT  549 

No  dilatation  to  Uic  right  iu  ordinary  type  of  adolescent 
dilatation  from  overstrain,  pp.  238,  354. 

Extreme  dilatation  to  the  right  may  be  superadded  to 
this  type  in  severe  valvular  disease  in  adolescence,  p.  (389). 

Age  as  a  factor  in  determining  the  type  of  upward  dilatation, 
pp.  290,  349. 

liower  border  of  the  cardiac  dullness  often  raised  by  rise 
of  the  diaphragm,  as  shown  by  the  level  of  the  gastric  resonance, 
pp.  181,  289. 

Rise  of  diaphragm  in  relation  to  the  shape  of  the  cardiac 
dullness,  pp.  246,  289. 

Lower  border  of  heart,  as  judged  by  position  of  apex  and 
area  of  pulsation,  may  be  raised  apart  from  rise  of  diaphragm. 

High  diaphragm  in  adolescent  dilatation  of  the  right 
ventricle,  explainable  in  other  cases  by  malnutrition  or  other 
cause  of  high  diaphragm,  p.  163. 

Two  cases  showing  high  apex  with  and  without  rise  of 
diaphragm  respectively,  pp.  (290),  (292). 

Frequency  of  upward  displacement  of  apex  in  adolescent 
heart  failure  of  anaemia,  pp.  234,  349. 

Statistics  as  to  the  frequency  of  tlie  various  phenomena 
associated  with  it,  pp.  349  to  356. 

Displacement  upwards  of  apex  due  to  its  upward  rotation 
by  a  slight  general  stretching  of  the  anterior  wall  of  the 
right  ventricle  towards  the  left,  pp.  237,  357. 

Upward  displacement  of  the  apex  more  common  in 
patients  over  nineteen  years  of  age  and  associated  with  a 
diminution  in  the  extreme  distensibility  of  the  upper  part 
of  the  right  ventricle  wall,  p.  349. 

Increase  of  cardiac  dullness  upwards  with  recumbency, 
pp.  266,  (298),  (305)  ;  sometimes  associated  with  a  corre- 
spondmg  rise  in  the  level  of  the  heart  apex,  p.  (313) ;  sometimes 
due  entirely  to  the  lessened  tension  of  the  anterior  wall  of 
the  ventricle  when  it  does  not  aid  in  supporting  the  weight 
of  the  heart,  and  without  any  rise  in  the  apex,  p.  (311). 

Increase  in  the  amount  of  dullness  in  the  second  and  third 
interspaces  with  shght  exertion  or  cardiac  excitement,  pp.  8,  (268), 

Bearing  of  this  increase  in  dullness  upon  the  cause  of  the 
pulmonary  systolic  murmur,  pp.  257,  268. 


550  SUMMARY 

Auscultation  of  the  veins  and  arteries  in  the  adolescent 
type  of  dilatation,  i.e.  in  '  heart  failure  with  enlargement  in 
distensible  hearts.' 

Auscultation  of  the  vems. 

Presence  of  a  '  britit  de  diable,'  especially  in  the  heart 
failure  of  anaemia,  pp.  15,  337. 

Its  characters  ;  louder  during  diastole  ;  disappearance  with 
recumbency,  pp.  16,  (285),  338  ;  causation  at  points  of  con- 
striction of  veins,  pp.  15,  337. 

Auscultation  of  arteries,  p.  226. 

Frequency  of  an  arterial  compression  murmur  in  the 
subclavians  in  the  adolescent  dilatation  of  ansemia,  pp.  226, 
281,  (299) 

Conduction  of  pulmonary  systolic  murmur  into  the  arteries 
of  the  neck,  especially  the  left  carotid,  pp.  215,  259,  335. 

Auscultation  of  the  Heart 

Pulmonary  Second  Sound. — Importance  of  notmg  the 
loudness  of  the  pulmonary  second  sound  as  giving  a  measure 
of  the  amount  of  extra  work  that  the  right  ventricle  is  doing — 
i.e.,  its  degree  of  overstrain  and  the  efficacy  of  its  muscular 
response  to  its  increased  load,  pp.  29,  42,  162,  337. 

Accentuation  of  pulmonary  second  sound  in  anaemic 
heart  failure,  pp.  244,  337,  415,  421. 

The  extremely  loud  second  sound  in  anaemic  heart  failure 
is  apparently  due  to  overstrain  caused  by  some  interference 
with  the  pulmonar}^  circulation  in  anaemia,  because  there  are 
no  evidences  of  left  ventricular  overstrain,  p.  245.  The  left 
ventricle  having,  apparently,  less  work  to  do  than  normal, 
p.  240. 

The  cause  of  hindrance  to  the  pulmonary  circulation  is 
uncertain,  pp.  246,  343. 

Pulmonary  second  sound  in  anaemia  is  louder  than  when 
the  right  ventricular  failure  is  secondary  to  left  ventricular 
failure  in  valvular  disease-,  pp.  244,  415,  421. 

Need  for  making  allowance  for  the  fact  that  in  adolescent 
dilatation  the  pulmonary  valves  are  closer  to  the  anterior  chest 
wall  tlian  normal. 

Eeduplication  of  the  second  sound. 


HEART  FAILURE  WITH  ENLARGEMENT  551 

Importance  of  noting  wliothfr  the  pulmonary  half  pre- 
cedes the  aortic,  or  vice  versa. 

In  ordinary  overstrain  in  adolescence,  and  especially  in 
anaemia,  the  pulmonary  half  precedes  the  aortic,  pp.  244, 
(297). 

When  right  ventricular  failure,  with  an  accentuated  pul- 
monary second  sound  with  reduplication  is  (say)  secondary 
to  left  ventricular  failure,  the  result  of  high  arterial  resistance, 
it  may  sometimes  be  noted  that  the  aortic  half  precedes 
the  pulmonary,  thus  giving  an  important  indication  for 
treatment. 

In  connection  with  the  effect  which  respiration  is  known 
to  have  on  the  action  of  the  right  ventricle,  it  is  of  interest 
to  note  that  careful  measurements  of  the  loudness  of  the 
pulmonary  second  sound  shows  that  the  second  sound  occurring 
with  the  first  cardiac  beat  after  the  commencement  of 
expiration  is  often  measurably  louder  than  the  rest,  p.  232. 

Loudness  of  the  right  ventricle  first  sound,  p.  244. 

It  is  important  to  note  the  loudness  of  the  fii'st  sound  heard 
over  the  right  ventricle  in  adolescent  heart  failure,  although 
there  are  other  indications  of  greater  value.  In  later  life  its 
diagnostic  value  is  great. 

Pulmonary  Artery  Systolic  Murmur,  p.  254 

A  most  valuable  sign  of  adolescent  heart  failure,  pp.  26,  215, 
254. 

Its  characters.     What  is  it  ? 

An  aneurysm-like  murmur  (sometimes  accompanied  by 
an  aneurysmal  thrill),  pp.  255,  334. 

It  accompanies,  but  does  not  replace  the  first  sound  of 
the  heart,  because  even  when  the  murmur  is  loud  the  first 
sound  usually  can  be  heard  quite  pure  over  the  lower  end  of 
the  sternum,  pp.  257,  259. 

It  has  rather  a  low  tone  as  a  rule— as  compared  with  a 
mitral  systolic  mm-mur,  for  instance,  p.  255. 

It  is  a  very  variable  murmur,  p.  256. 

It  varies  very  greatly  with  change  of  position,  being  often 
quite  loud  when  the  patient  is  recumbent  and  faint  or  absent 
when  erect,  pp.  256,  266. 


552  SUMMARY 

It  is  always  increased  with  rocunibeiicy,  pp.  256,  334. 

It  is  greatly  increased  in  loudness  by  slight  exertion, 
p.  257. 

It  is  greatly  increased  in  loudness  by  excited  heart  action, 
pp.  257,  (268)." 

It  can  sometimes  be  noticed  to  vary  in  loudness  with 
respiration,  just  as  is  the  case  with  the  pulmonary  second  sound. 

It  varies  according  to  the  strength  of  the  heart  rather 
more  than  an  ordinary  valvular  murmur.  It  may  l3e  faint 
when  the  heart  is  weak,  and  rapidly  gain  in  loudness  in  a  few 
days  as  the  heart's  strength  improves,  p.  263. 

In  the  same  way  a  very  loud  murmur  may  very  rapidly 
lessen  in  loudness  in  a  week  or  two  on  the  improvement  of 
the  heart,  fig.  75,  p.  261. 

When  is  the  murmur  audible  ? 

It  is  systolic  in  rhythm  and  apparently  accompanies  the 
first  sound  of  the  heart.  If  accurate  measurement  were  possible 
it  would  probably  be  found  to  commence  just  after  the  closure 
of  the  auriculo-ventricular  valves  and  attain  its  maximum 
when  the  pulmonary  artery  reaches  its  fullest  (i.e.  at  the  time 
when  the  recoil  wave,  due  to  its  elasticity,  returns  into  the 
ventricle),  p.  257. 

Where  is  the  murmur  audilde  ? 

Its  point  of  maximal  intensity  (its  P.M.I.)  appears  to 
coincide  with  the  situation  of  the  pulmonary  artery,  p.  258. 

In  slight  cases  of  adolescent  dilatation  this  may  be  in 
about  the  normal  situation  at  the  sternal  end  of  the  second 
left  interspace,  p.  260. 

Sometimes  in  extreme  cases  the  artery  (and  the  P.M.I,  of 
the  murmur)  may  be  1  or  1|  inches  away  from  the  sternum, 
p.  258. 

The  situation  of  the  pulmonary  artery  may  sometimes  be 
shown  by  the  shock  due  to  the  closure  of  the  semilunar 
valves  being  palpable,  pp.  232,  (286),  332. 

The  P.M.I,  of  the  murmur  may  sometimes  be  noticed  to 
change  a  little  with  change  of  posture — as  is  the  case  with 
the  P.M.I,  of  the  pulmonary  second  sound  (due  to  the  increase 
in  the  amount  of  upward  dilatation  which  recumbency  causes), 
p.  258. 


PULMONARY  SYSTOLIC  MURMUR  553 

Its  direction  of  conduction,  pp.  215.  25it.  :W5. 

When  moderately  loud  it  is  heard  over  an  area  a  few 
inches  aci-oss,  spreading  upwards  and  outwards  from  its  P.M.L, 
}).  260. 

Not  heard  l)elow  tlie  fourth  lib.  (When  apparently  heard 
lower  down  this  is  really  an  independent  tricuspid  murmui'), 
pp.  2.-)!),  (27H). 

Not  well  heard  to  the  right  of  the  sternum  unless  very 
loud.  (When  apparently  conducted  to  the  right  this  is  reallj'' 
an  independent  superior  vena  cava  murmur.) 

Sometimes  conducted  up  into  the  neck  and  then  is  usually 
])etter  heard  in  the  left  carotid  than  the  right.  (This  is  due 
to  the  close  contact  of  the  dilated  pulmonary  artery,  in  which 
the  murmur  arises,  with  the  second  part  of  the  arch  of  the 
aorta,  pp.  215.  2.59.  335. 

How  is  the  pulmonary  sj'stolic  murmur  caused  ? 

The  clinical  evidence  shows  that  it  is  a  murmur  of  right 
ventricular  origin,  pp.  26.  263. 

That  it  does  not  arise  at  the  tricuspid  valve,  pp.  259,  263. 

That  its  cHnical  features  all  suggest  the  pulmonary  arter}'^ 
as  its  point  of  origin. 

Theory  as  to  its  mode  of  origin  in  the  pulmonary  artery. 
The  murmur  results  from  the  pulmonary  artery  losing  its 
normal  cylindrical  form  and  becoming  more  or  less  spherical 
when  the  elastic  tissue  which  constitutes  its  wall  is  inadequate 
to  resist  the  blood  pressure  developed  within  the  artery  hj 
the  right  ventricle,  pp.  270,  335. 

In  other  words,  the  murmur  arises  in  a  temporary  aneurysm- 
like  dilatation  of  the  pulmonary  artery,  pp.  26.  252,  336. 

Such  a  dilatation  can  arise — 

1.  Simply  from  an  excess  of  blood  pressure  in  an  artery 
whose  elastic  wall  is  practically  normal,  p.  273. 

This  rarely  happens.  Kecords  of  such  a  case,  pp.  (274)  and 
(300). 

2.  From  relaxation  of  the  arterial  wall  lessening  its  resisting 
power.     This  is  the  ordinary  cause  of  the  murmur,  pp.  26,  272. 

3.  This  theory  necessitates  a  blood  pressure  adequate  to 
cause  dilatation  of  the  artery,  pp.  27,  272. 

4.  A  pulmonary  orifice  smaller  in  size  than  that  of  the 


554  SUMMARY 

vessel  when  dilated  ;  otherwise  the  pulmonary  artery  could 
not  constitute  an  aneurysmal  dilatation,  but  only  a  cylindrical 
prolongation  of  the  cavity  of  the  conus  arteriosus  in  which 
no  murmur  would  arise,  pp.  27,  272,  275. 

5.  In  addition  to  the  above-mentioned  factors,  the  forma- 
tion of  murmur-producing  eddies  in  the  dilated  artery  is 
facilitated  by  the  fact  that  the  upward  dilatation  of  the  right 
ventricle,  which  causes  the  murmur,  results  in  an  alteration 
in  the  axis  of  the  pulmonary  artery  as  compared  with 
that  of  the  ventricle,  the  blood  being  projected  against  its 
anterior  wall  and  not  directly  into  its  lumen  as  in  the  normal 
heart,  pp.  252,  271,  336. 

The  ordmary  phenomena  already  described  are  easily 
explained  by  the  variations  in  the  blood  pressure  and  by  the 
variations  in  the  degree  of  relaxation  of  the  elastic  w^all  of  the 
j)ulmonary  artery. 

A  lessening  in  the  loudness  of  the  murmur,  owing  to  dila- 
tation of  the  pulmonary  orifice,  is  seen  in  cases  of  extreme 
adolescent  dilatation,  pp.  264,  275. 

Variations  in  the  murmur  due  to  any  variation  m  the 
direction  of  the  pulmonary  artery  are  neither  likely  to  occur 
nor  likely  to  be  of  clinical  importance. 

The  Clinical  Characteristics  of  the  pulmonary  systolic 
murmur  harmonise  with  the  above  theory. 

The  murmur  is  of  an  aneurysmal  type,  p.  255. 

The  extreme  and  rapid  variability  of  the  murmur  suggests 
its  production  in  an  elastic  structure — such  as  the  pulmonary 
artery — which  can  readily  recover  itself  on  the  removal  of  a 
disturbing  factor,  p.  263. 

Variations  in  the  Amount  of  Relaxation  of  the 
pulmonary  artery. 

The  conditions  resulting  from  upward  dilatation  of  the 
right  ventricle  are  such  as  to  produce  an  amount  of  relaxation 
adequate  to  give  rise  to  a  murmur,  pp.  251,  336. 

The  raising  of  the  level  of  the  pulmonary  valves  by  the 
upward  dilatation  of  the  ventricle  will  approximate  the  com- 
mencement of  the  pulmonary  artery  to  its  termination  at 
its  bifurcation — the  latter  being  a  fixed  point.  The  arterial 
wall  will  thereby  be  relaxed,  p.  249. 


PULMONARY  SYSTOLIC  MURMUR  555 

The  relaxation  will  be  directly  proportional  to  the  amount 
of  upward  dilatation,  and  if  the  other  variable  factors  are  con- 
stant the  loudness  of  the  murmur  ought  to  be  proportional  to 
the  amount  of  upward  dilatation,  pp.  26,  264. 

This  is  found  to  be  the  case  clinically ;  for  the  loudness  of 
the  murmur  and  the  amount  of  upward  dilatation  are  both 
increased  by  : — 

1.  Change  of  posture ;  recumbency  causing  a  marked 
increase,  pp.  27,  266. 

2.  Excited  action  of  the  heart,  pp.  228,  257,  268. 

3.  Slight  amounts  of  exertion,  p.  268. 

4.  Also  in  a  series  of  cases  (if  those  be  excluded  where 
there  is  a  likelihood  that  the  pulmonary  orifice  is  becommg 
dilated),  the  loudness  of  the  pulmonary  systolic  murmur  is 
found  to  be  proportional  to  the  amount  of  upward  dilatation 
present,  p.  264. 

Variation  in  the  Blood  Peessuee  as  a  factor  in  the 
causation  of  the  murmur  also  confirms  the  above  theory. 

The  strildng  variations  in  the  loudness  of  this  murmur  are 
due  to  the  fact  that  any  sudden  increase  of  blood  pressure — such 
as  results  from  slight  exertion  or  excited  action  of  the  heart 
from  emotional  or  other  causes — not  only  increases  the  distensile 
pressure  which  the  right  ventricle  develops  in  the  pulmonary 
artery  at  each  systole,  but  also  (owing  to  the  distensibility 
of  the  upper  part  of  the  ventricle  wall  in  adolescence)  such 
increase  in  the  heart's  activity  also  increases  the  amount  of 
upw^ard  dilatation,  and  therefore  the  degree  of  relaxation  of 
the  artery.  Increased  cardiac  activity  therefore,  has  the 
double  effect  of  increasing  both  the  relaxation  of  the  arterial 
wall  and  the  distensile  force,  pp.  268,  272. 

Presence  of  accentuation  of  pulmonary  second  sound  of 
value  in  estimating  the  strength  of  the  right  ventricle,  pp.  244, 
269. 

When  the  heart  nniscle  is  too  weak — as  in  severe  cases 
of  simple  anaemia — to  develop  an  adequate  distensile  force, 
a  considerable  amount  of  upward  dilatation  may  be 
accompanied  b}'^  but  a  faint  murmur,  p.  273. 

In  such  a  case,  return  of  cardiac  strength  will  bo  accom- 


556  SUMMARY 

paiiicd  by  increased  loudness  of  the  murmur,  and  it  will  then 
become  proportional  to  the  amount  of  dilatation,  p.  (305). 

In  such  a  case  as  this,  the  return  of  cardiac  strength  will 
often  be  accompanied  by  a  decided  increase  in  the  amount 
of  dilatation,  pp.  (294),  (297),  (304). 

Briefly,  it  can  be  said  that  with  a  constant  blood  pressure 
in  the  artery  the  loudness  of  the  murmur  will  be  proportional 
to  the  degree  of  relaxation  caused  by  the  upward  dilatation 
of  the  ventricle,  or  with  a  constant  degree  of  relaxation  of 
the  vessel  wall  the  loudness  of  the  murmur  will  be  directly 
j)roportional  to  the  amount  of  the  blood  pressure. 

Variation  in  loudness  of  murmur  with  varying  cardiac 
strength,  p.  (304). 

In  confirmation  of  this  it  may  be  noticed  that  in  the  excep- 
tional cases  where  the  murmur  is  not  due  to  relaxation  of  the 
arterial  wall  or  where  the  anterior  wall  is  sufficiently  strong 
for  its  amount  of  dilatation  not  to  be  lessened  in  the  erect 
attitude,  the  slight  increase  in  cardiac  activity  which  the 
erect  attitude  calls  out,  is  sufficient  to  make  the  pulmonary 
murmur  louder  in  the  erect  than  in  the  recumbent  attitude, 
pp.  (274)  and  (300). 

Cases  where  the  murmur  was  not  increased  on  lying  down, 
pp.  (300),  (302),  (303). 

Accentuation  of  pulmonary  second  sound  lessened  on 
lying  down,  p.  300. 

Variations  in  the  Size  of  the  Pulmonary  Orifice 

For  the  production  of  murmur-producing  eddies  it  is 
necessary  that  the  orifice  of  entrance  be  smaller  than  the 
chamber  in  which  the  eddies  are  to  be  produced,  p.  271. 

It  may  therefore  be  stated  that,  other  factors  being  constant, 
the  loudness  of  the  pulmonary  murmur  will  be  proportional 
to  the  smallness  of  the  pulmonary  orifice  in  comparison 
with  the  size  of  the  dilated  artery,  and  conversely  when  the 
size  of  the  pulmonary  orifice  approaches  that  of  the  dilated 
pulmonary  artery  the  production  of  a  murmur  is  no  longer 
possible. 

In  a  series  of  cases  where  there  is  ver}^.  extreme  upward 


HEART  FAILURE  WITH  ENLARGEMENT  557 

dilatation  of  the  right  ventricle  it  k  found  that  the  puhnonary 
artery  murmur  is  often  faint  or  oven  quite  absent,  pp.  264, 
275,  (306),  (314). 

Lessening  of  puhnonary  murmur  with  increase  of  heart 
vigour  and  of  dilatation,  pp.  ('294),  (304). 

In  further  confirmation  of  tliis  theory,  it  is  sometimes 
found  that  when  once  the  pulmonary  murmur  has  disappeared 
(owing  to  the  stretching  of  the  pulmonary  orifice),  it  does  not 
reappear  when  the  upward  dilatation  of  the  ventricle  lessens. 
In  such  a  case,  we  shall  iind  the  murmur  absent,  in  spite  of 
there  being  a  moderate  amoimt  of  upward  dilatation — such  an 
amount  as  is  usually  accompanied  by  a  loud  murmur,  p.  297. 

Another  possible  factor  must  be  referred  to — namely,  that 
in  cases  of  extreme  dilatation  the  support  given  by  surround- 
ing structures  may  to  some  extent  lessen  the  aneurysmal 
dilatation  of  the  pulmonary  artery,  pp.  27,  276. 

Other  Auscultatory  Phenomena  sometimes  found  in 
the  adolescent  type  of  dilatation. 

A  third  sound  of  the  heart,  audible  over  the  right 
ventricle  may  be  heard,  pp.  282,  340. 

Position  of  interventricular  septum  shown  by  the  area 
of  audition  of  the  third  sound,  pp.  284,  341. 

Effect  of  change  of  position  on  the  third  sound,  p.  284. 

Third  sound  only  audible  when  recumbent,  p.  (313). 

Mid-diastolic  tricuspid  murmur  audible  in  right  ventricular 
dilatation — especially  in  anaemic  heart  failure,  pp.  282,  (283), 
341. 

Arterial  compression  murmur  (especially  in  anaemia),  pp.  226, 
281,  (299). 

Tricuspid  systolic  murmur  infrequent  in  anaemia,  p.  239. 

Sequence  of  clinical  phenomena  observable  in  gradually 
increasing  degrees  of  cardiac  failure,  pp.  28  to  30. 

Cardiac  Failure  with  Enlargement  in  Moderately 
Distensible  Hearts,  i.e.  Adult  Type  of  Dilatation, 
p.  47 

The  Clinical  Phenomena  are  those  usually  described  as 
characterising  heart  failure. 
Symptoms,  p.  36. 


558  SUMMARY 

Breathlessness  more  important  in  aduit  life  than 
adolescence,  p.  36. 

Pain,  p.  37.  Greater  liability  to  cardiac  pain  in  adnlt  than 
adolescent. 

Other  symptoms — cyanosis,  dropsy,  &c. 

Physical  Signs  relating  to  the  right  ventricle. 

Inspection.  Increase  of  pulsation  just  to  left  of  sternum, 
p.  40. 

Later  on,  pulsation  to  the  right  of  sternum  and  in  the 
epigastrium,  p.  40. 

Fullness  and  pulsation  of  the  veins  of  the  neck,  p.  38. 

False  pulsation  at  first,  true  pulsation  later  on,  pp.  39, 
137,  338. 

Information  from  radial  pulse.  Its  unreliability  in  adult 
and  later  hfe,  pp.  35,  (35),  143. 

Force  and  volume  of  the  impulse  in  jugular  bulb  of 
great  value  in  estimating  the  amount  of  cardiac  failure, 
p.  39,  134. 

Force  and  volume  of  systolic  pulsation  in  neck  veins  (if  any) 
also  of  importance,  p.  135. 

Character  and  position  of  apex  beat  to  be  observed. 

Presence  of  abnormal  pulsation  just  to  left  of  sternum  and 
its  force  to  be  noted,  pp.  17,  29,  40. 

Also  extension  of  area  of  pulsation  to  the  right  or 
downwards,  or  in  severe  cases,  pulsation  of  the  liver,  p.  40. 

Case  of  right  ventricle  failure  with  venous  plethora,  but 
no  dilatation  to  the  right,  fig.  91,  p.  278. 

Percussion  of  the  heart.  Shows  the  measm'e  of  dilatation 
to  the  left  and  to  the  right  with  greater  exactness  than 
palpation,  p.  25. 

Auscultation,  p.  26,  of  the  veins,  pp.  24,  219,  (291). 

The  'points  to  he  noted  in  connectioyi  with  the  heart  are : — 

Study  the  relative  loudness  of  right  ventricle  first  sound 
as  compared  with  the  left.  Also  the  loudness  of  the  pul- 
monary (p.  29)  and  aortic  second  sounds.  If  reduphcation 
be  present  notice  which  half  of  the  second  sound  occurs 
first,  as  indicating  whether  the  right  heart  or  the  left  be 
more  overstrained. 

Note  the  presence  or  absence  of  murmurs. 


TRICUSPID  REGURGITATION  559 

In  early  heart  failure  the  presence  of  a  pulmonary  systolic 
murmur  in  early  adult  life  may  be  noted,  p.  26. 

Of  most  importance  are  the  signs  of  tricuspid  regurgitation, 
p.  8.  A  third  sound  and  mid-diastolic  murmur  may  occur 
in  right  ventricular  dilatation,  pp.  46,  282. 

Tricuspid  Eegurgitation 

A  sign  of  heart  failure. 

Due  to  dilatation  of  basal  part  of  ventricle,  pp.  32,  37. 

Compensatory  effect  of  it  in  limiting  dilatation,  p.  32. 
Its  effect  on  right  auricle,  p.  41. 

Tonic  muscular  response  by  wall  of  auricle,  pp.  509,  521,  585. 
Dilatation  of  auricle,  and  see  '  Auricle  '  in  subject  index, 

p.  210. 
A  dilated  auricle  does  not  as  a  rule  come  near  anterior 
chest  wall,  p.  41. 
Its  effect  upon  the  great  veins  forming  a  part  of  the  auriculo- 
venous  reservoir. 
Tonic  muscular  response  by  their  walls,  pp.  507,  513,  586. 
Degree  of  fullness  of  auriculo -venous  reservoir  shown  by 

the  volume  of  the  pulsation  felt  in  jugular  bulb,  p.  132. 
Chronicover-distension  causing  descent  of  diaphragm,  p.  362. 
In  other  ways,  vide  Summary — '  Auriculo-venous  Reservoir.' 
Force  with   which  the  reservoir  is   distended  judged  by 
the  strength  of  the  pulsation  in  the  jugular  bulb,  pp.  133, 
137. 
Its  relation  to  the  inferior  and  superior  vena  cava,  pp.  37.  210. 

Importance  of  the  Eustachian  valve,  p.  38. 
Regurgitation  downwards  into  the  liver,  p.  39. 
Clinical  changes  in  liver  which  result. 
Enlargement,  pp.  39,  210. 
Effect  of  over-distension  upon  percussion  dullness,  pp.  24, 

191. 
Increased  conductivity  to  intestinal  resonance  is  caused 

by  venous  engorgement,  pp.  24,  191. 
Pulsation  of  the  liver,  p.  210. 
Pain  due  to  over-distension  of  the  liver,  p.  37. 
Ascites. 


560  SUMMARY 

Kegurgitation  upwards  into  llio  superior  vena  cava. 
Its  effect  upon  the  superior  vena  cava,  pp.  44,  218. 
Its  effect  upon  the  veins  of  the  neck,  p.  39. 
Fullness  and  false  pulsation  when  slight,  p.  38. 
Fullness  and   false    pulsation   when   Aentricle  muscularly 

weak,  p.  137. 
Systolic  pulsation  in  the  neck  veins,  p.  132. 
Ehythm  of  the  pulsation,  p.  135. 

Sometimes  so  forcible  as  to  resemble   arterial  pulsation, 
pp.  (220),  (222). 
Its  clinical  recognition  in  other  ways. 

Usually   associated   with   increase   of   cardiac  dullness   to 

the  right  of  the  sternum,  pp.  40,  (321),  (339). 
Often  with  pulsation  to  the  right  of  the  sternum. 
Sometimes  there  is  no  pulsation  either  in  neck  veins  or 
Uver,  p.  339. 

AUSCULATORY  SIGNS. 

A    SYSTOLIC    MURMUR   may  be  produced  by  tricuspid  regur- 
gitation in  either  or  all  of  three  situations,  pp.  43,  217, 
338. 
At  the  tricuspid  valve. 

The  tricuspid  systohc  murmur,  pp.  43,  217,  339. 

Its  occurrence.  Not  always  present,  p.  43  ;  absent  in 
spite  of  dilatation  of  ventricle  and  regurgitation, 
pp.  (278),  (280),  (320). _ 

Similar  absence  of  sj^stolic  mitral  murmur  in  case  of  great 
dilatation  of  the  left  ventricle,  pp.  (281),  (320). 

Its  character,  P.M.I.,  &c.,  pp.  43,  217,  339. 

Variation  with  attitude  of  patient.  Usually  less  loud  when 
erect.   Absent.   Fig.  73,  pp.  261,  (303).    No  change,  p.  301. 

Variation  with  respiration,  p.  500. 

Area  of  audition,  pp.  43,  339. 

Propagation  downwards  towards  liver,  pp.  44,  218,  339. 

Propagation  upwards  into  veins,  pp.  (221),  223. 

Propagation  towards  the  back,  p.  445. 

Diagnostic  importance  of  noting  relationship  of  right 
ventricle  first  sound  to  a  true  tricuspid  systolic  murmur, 
pp.  218,  223. 


TRICUSPID  REGURGITATION  561 

In  the  supeeiok  vena  cava. 

The  superior  vena  cava  mui'mur,  pp.  44,  218. 

Effect    of   regurgitation"  upon    the    superior    vena    cava. 

Its   dilatation  results  in  a  relative  constriction  by  the 

unyielding  fibres  of    the  pericardium  where   it  passes 

through  it,  p.  44. 
Characters  of  this  murmur. 
Somewhat  similar  to  those  of  the  tricuspid  murmur,  pp. 

45,  218. 
Point    of   maximum   loudness.     Third    and    second    right 

interspaces,  pp.  45,  218. 
Conduction  into  veins  of  neck,  pp.  45,  219. 
Diagnosis  from  a  true  tricuspid  murmur,  p.  45. 
Diagnosis  from  an  aortic  systolic  murmur,  pp.  45,218,(222). 
Similarity  to  an  aortic  systolic  murmur,  p.  221. 
Diagnosis  from  a  pulmonary  systolic  murmur,  vide  pp.  219 

and  334. 
Its  diagnostic  importance — especially  in  heart   failure  of 

later  life,  pp.  46,  87. 
Superior    vena  cava  murmur  and  no    tricuspid  murmur, 

pp.  (222),  (224),  (320). 
Superior  vena  cava  murmur  in  pneumonia  with  no  distinct 

signs  of  dilatation  of  right  ventricle,  p.  (224). 

At  the  Venous  Valves. 

Venous  valve  murmur,  p.  219,  590. 

Produced  by  incompetence  of  the  venous  valves. 

Rough  quality  of  the  murmm-. 

Occurrence  of  a  thrill. 

Point  of  maximal  intensity  over  site  of  origin. 

Differential  diagnosis  easy. 

Venous  valvular  murmur  in  jugular  vein,  p.  (291). 

A  Summary  and  Index  of  Arguments  and  Facts  brought 

FORWARD    IN    CONNECTION  WITH    PHYSICAL    SiGNS    RELAT- 
ING TO  THE  Left  Ventricle,  p.  46 
Early  diagnosis  of  failm-e  of  left  ventricle  is  not  so  easy  as 
that  of  the  right  owing  to  its  anatomical  situation  deep  in  the 
chest,  pp.  2,  47. 

20 


562  SUMMARY 

The  signs  of  loft  ventricular  failure  are  the  well-recognised 
ones  of  dilatation  and  mitral  systolic  murmur. 

The  lessened  cardiac  distonsibility  characteristic  of  adult 
life  is  shown  by  the  increased  frequency  with  which  signs  of 
dilatation  of  the  left  ventricle  occur  in  overstrain,  as  compared 
with  early  life.  Also  by  the  occurrence  (with  or  without 
left  ventricular  dilatation)  of  the  ordinary  type  of  dilatation 
of  the  right  ventricle  towards  the  right  with  signs  of  tricuspid 
regurgitation,  pp.  11,  47,  309. 

The  tendency  for  the  right  ventricle  to  dilate  before  the 
left  (and  especially  if  upward  dilatation  of  the  right  ventricle 
also  be  present)  shows  the  possession  still  of  some  measure 
of  adolescent  distensibility,  p.  33. 

On  the  other  hand,  a  tendency  of  heart  failure  to  be  accom- 
panied by  less  dilatation  of  the  right  ventricle  than  might 
reasonably  be  expected  (considering  the  degree  of  overstrain 
of  the  left)  shows  the  onset  of  the  relative  rigidity  which  is 
characteristic  of  later  life.  The  occurrence  of  less  dilatation  of 
either  ventricle  than  might  reasonably  be  expected  shows  a 
further  degree  of  this  same  relative  rigidity,  unless  there  be 
evidences  of  myocardial  weakness  to  account  for  the  relative 
absence  of  dilatation,  p.  147. 

In  the  same  mamier  a  complete  absence  of  dilatation  of  the 
left  ventricle,  in  spite  of  overstrain,  in  a  heart  strong  enough 
to  make  dilatation  reasonably  probable,  is  an  evidence  of  a 
considerable  degree  of  the  rigidity  of  later  life,  p.  86. 

The  mitral  systolic  murmur  a  sign  of  dilatation  of  the 
left  ventricle,  p.  47. 

Its  diagnosis  from  a  tricuspid  systolic  murmur,  p.  48. 

Its  diagnosis  from  car dio -respiratory  murmm^s,  p.  49,  446. 

Sometimes  absent  in  spite  of  great  dilatation,  pp.  (277),  (281), 
(320). 

Heart  Failure  in  Valvular  Disease 

Dilatation  and  hypertrophy  necessary  for  compensation  in 
valvular  disease,  pp.  47,  389. 

Importance  of  distensibility  for  the  development  of  com- 
pensation, pp.  11,  452. 


VALVULAR  DISEASE  563 

Serious  results  of  valvular  disease  in  later  life  or  in  adherent 
pericardium  where  the  ventricle  is  too  rigid  to  dilate,  pp.  150, 
(433),  (454),  (455),  (456). 

Estimation  of  degree  of  rigidity  of  the  heart  wall  in 
valvular  disease,  p.  150. 

Liabihty  of  mistaking  pallor  due  to  faulty  compensation 
for  simple  anaemia,  p.  453. 

See  also  '  Compensation  for  Valvular  Disease  '  (p.  594)  and 
'  Mid-diastolic  Murmur  '  and  '  Third  Sound  of  Heart  '  in  subject 
index. 

Mitral  Systolic  Murmur  due  to  organic  valvular  disease. 

Conduction  of  mitral  systolic  murmur  down  the  spine, 
p.  442. 

Kelationship  of  left  auricle  to  vertebrae,  p.  443. 

Estimation  of  amount  of  regm-gitation  by  audibility  of 
the  mm-mm-  down  the  spine,  pp.  444,  447. 

Prognostic  value  of  the  degree  of  audibihty  of  the  mitral 
systolic  murmur  over  the  lumbar  vertebrte,  p.  447. 

Evidences  of  the  onset  of  muscular  failure  in  hearts  enlarged 
by  valvular  disease,  p.  110. 

Amongst  the  more  evident  signs  may  be  noted  : — 

Defective  compensatory  dilatation  of  the  heart  where 
there  is  no  reason  to  suspect  rigidity  of  the  heart  wall  is  an 
indication  of  myocardial  weakness,  pp.  (65),  150. 

Diminution  in  the  size  of  a  heart  enlarged  by  compen- 
satory dilatation  and  hypertrophy  is  a  sign  of  deterioration 
of  the  heart  muscle,  pp.  62,  110,  (316). 

Lessened  cardiac  dilatation  in  aortic  regm'gitation  an 
evidence  of  myocardial  weakness,  p.  (112). 

A  lessening  in  the  size  of  a  hver  enlarged  by  chronic  venous 
congestion  may  be  a  sign  of  myocardial  failure  as  well  as  of 
improvement  of  the  heart,  pp.  Ill,  112. 

A  sudden  diminution  in  size  of  an  enlarged  liver  may  be 
a  sign  of  sudden  heart  weakness  in  valvular  disease,  pp.  (63) 
and  (-201). 


504  SUMMARY 


A  Summary  and  Index  of  xVkuumbnts  and  Facts  brought 

FORWARD  IN  CONNECTION   WITH  HeART  FaILURE  WITHOUT 

Enlargement,  p.  50 

The  force  producing  dilatation  must  be  the  force  developed 
by  the  ventricular  contraction,  p.  6. 

When  the  resisting  power  of  the  heart  walls  is  greater 
than  the  intraventricular  pressure  Avhich  the  ventricle  can 
develop,  no  dilatation  is  possible  ;  hence  in  these  cases  heart 
failure  without  enlargement  must  result,  pp.  5,  50,  86,  91. 

The  inefficiency  of  the  intraventricular  pressure  may  be 
due  to  : — 

Abnormally  resistant  heart  walls  (see  '  Heart  Failure 
without  Enlargement  in  Moderately  Strong  Hearts'),  pp.  86, 
(87),  (89). 

Abnormally  weak  cardiac  muscle,  pp.  51,  54. 

Often  both  factors  are  at  work,  and  the  part  played  by 
each  is  not  always  easily  determined,  pp.  79,  81,  91,  96,  147. 

When  there  is  an  absolute  inefificiency  in  the  ventricular 
force — owing  to  muscular  weakness — the  amount  of  blood 
expelled  at  each  beat  (in  the  face  of  a  normal  or  an  increased 
arterial  resistance)  must  be  lessened  proportionally  to  the 
lessening  in  the  heart's  expulsive  power,  pp.  51,  55. 

In  spite  of  this  lessened  output  by  the  ventricle,  over- 
distension of  the  veins  does  not  usually  occur.  The  veins  are, 
on  the  other  hand,  abnormally  empty  as  a  rule  in  myocardial 
weakness  ;  consequently,  when  myocardial  weakness  is  well 
marked  there  must  be  a  compensatory  lessening  of  the  volume 
of  blood  in  active  circulation,  proportional  to  the  deficiency  in 
the  amount  expelled  by  the  ventricles  (see  '  Blood  Volume, 
Compensatory  Lessening  of  '  p.  577),  pp.  53,  132. 

Where  the  heart  wall  is  sufficiently  soft  and  yielding,  this 
lessened  intraventricular  pressure  and  lessened  output  is 
accompanied  by  a  diminution  in  the  size  of  the  heart — as 
observed  clinically — which  is  proportional  to  the  degree  of 
muscular  weakness  present. 

A  group  of  cases  must,  therefore,  be  recognised  in  which 
there  is — 


HEART  FAILURE  WITH  SMALL  HEART  565 

Heaet  Failure  with  Fmall  Heart,   p.  54 

Compensatory  diminution  in  the  size  of  the  heart  results 
in  another  compensatory  advantage — namely,  a  lessening  in 
the  sectional  area  of  the  ventricle  at  the  onset  of  its  contrac- 
tion, whereby,  on  the  principle  of  the  hydraulic  press,  the 
discharge  of  its  contents  into  the  aorta  is  facilitated  (the  sectional 
area  of  the  aorta  orifice  is  not  likely  to  be  correspondingly 
lessened),  p.  52. 

Mechanism  bringing  about  compensatory  diminution  in 
the  size  of  the  heart,  p.  52. 

The  fullness  of  a  heart  depends  upon  its  power  of  hlling 
itself  by  the  aspiratory  force  of  its  expansion. 

The  force  of  its  expansion  is  directly  dependent  on  its 
muscular  power  both  as  regards  muscular  expansion  and 
elastic  recoil,  p.  53. 

In  the  case  of  muscular  expansion,  heart  muscles  which 
are  too  Aveak  to  develop  adequate  contractile  force  must  be 
still  more  inadequate  as  regards  expansile  force,  p.  52. 

In  the  case  of  mechanical  elastic  recoil,  the  vigour  of  the 
recoil  must  be  dependent  upon  the  vigour  of  the  contraction 
causing  the  recoil  and  must  l)e  somewhat  less  vigorous  when 
the  heart  muscle  is  weak,  p:   53. 

Therefore,  in  a  heart  which  fills  itself  mainly  by  its 
muscular  aspiraticn — when  the  heart  muscle  is  weak — its 
power  of  filling  itself  will  be  at  least  as  defective  as  its 
power  of  emptying  itself,  p.  53. 

In  Adolescence. 

Therefore,  in  early  hfe  when  (owing  to  the  immaturity 
of  the  fibrous  tissues)  the  heart  does  depend  almost  entirely 
upon  its  muscular  aspiration  (p.  183),  incomplete  filhng  may 
be  expected  to  be  proportional  to  the  inefficacy  of  its  expulsive 
power,  p.  53. 

Therefore,  well-marked  and  adequate  compensatory  dimin- 
ution in  the  size  of  the  heart  will  accompany  myocardial 
weakness,  p.  56. 

Clinically,  in  adolescence,  marked  diminution  in  the  size 
of  the  heart  is  found  in  cases  of  myocardial  weakness.     The 


566  SUMMARY 

smallness  of  tho  heart  appears  to  bo  proportional  to  the  amount 
of  weakness  present,  pp.  (65),  (68). 

In  iVdult  and  Later  Life. 

In  hearts  possessing  elastic  recoil  in  addition  to  muscular 
expansion,  less  extreme  interference  with  the  filling  of  the 
heart  will  occur,  and,  therefore,  compensatory  diminution  in 
the  size  of  the  heart  will  be  less  complete  in  adult  and  later 
life  than  in  adolescence,  pp.  54,  73,  80. 

The  greater  the  amount  of  elastic  recoil  possessed  by  the 
heart  the  less  perfect  will  the  compensatory  incompleteness 
of  the  filling  of  the  heart  and  the  less  its  reduction  in  size, 
p.  80. 

As  the  possession  of  elastic  recoil  depends  upon  the  rigidity 
or  otherwise  of  the  fibrous  elements  of  its  wall  (i.e.  its  dis- 
tensibility),  it  can  be  asserted  that  the  distensibihty  of  a  heart 
that  is  muscularly  weak  may  be  estimated  b}^  the  amount  of 
diminution  in  the  size  of  the  heart  that  occurs  for  any  given 
degree  of  mj'ocardial  weakness.  The  distensible  heart  will 
show  much  diminution  ;  the  relatively  rigid  one  but  little, 
p.  81. 

Compensatory  diminution  in  the  size  of  the  heart  is  inter- 
fered with  in  another  manner  by  the  maturity  of  the  filirous 
tissues  upon  which  the  possession  of  elastic  recoil  depends. 
This  same  maturity  (or  relative  rigidity)  of  the  tissues  of  the 
heart  wall  tends  to  make  it  retain  its  normal  size  and  shape, 
instead  of  remaining  only  partly  filled,  as  in  the  case  where 
its  tissues  are  softer,  p.  79. 

In  later  life,  where  a  considerable  degree  of  this  rigidity 
may  occur,  there  may  be  no  lessening  at  all  of  the  size  of  the 
heart  in  myocardial  weakness  ;  just  as  under  similar  circum- 
stances heart  failure  in  a  strong  heart  may  occur  ^^^thout 
any  dilatation,  p.  80. 

It  may,  therefore,  be  asserted  that  the  distensibihty  of 
the  heart  in  adolescence  and  early  life  is  shown  by  the  degree 
to  which  the  moderately  strong  heart  dilates  in  the  face  of 
overstrain  and  by  the  degi'ee  in  which  the  weak  heart 
diminishes  in  size  on  the  occurrence  of  myocardial  weakness, 
p.  81. 


HEART  FAILURE  WITHOUT  ENLARC4EMENT     567 

The  degree  of  rigidity  of  the  heart  in  adult  and  later  life 
is  shown  by  the  extent  to  which  a  strong  heart  fails  to  dilate 
under  circumstances  that  might  be  reasonably  expected  to 
produce  dilatation,  pp.  8G,  (87). 

Or,  in  the  case  of  a  weak  heart,  by  the  extent  of  its  failure 
to  diminish  in  size  in  the  face  of  well-marked  myocardial 
weakness,  p.  81. 

Certain  consequences  follow  this  imperfect  compensatory 
diminution  in  size. 

The  compensatory  diminution  in  the  size  of  the  ventricle 
being  less  complete  than  in  a  softer  heart  there  will  be 
incomplete  emptying  of  the  ventricle  with  each  systole,  p.  82. 

The  possession  of  elastic  as  w^ell  as  muscular  aspiration 
will  render  the  ventricle  liable  to  draw  into  itself  more  blood 
than  it  is  able  to  expel,  p.  53. 

In  adolescence  and  early  life,  anginal  pain,  from 
ventricular  over-distension,  is  extremely  rare — apart  from 
valvular  disease — because  the  heart  cannot  overfill  itself.  If 
too  weak  to  empty  itself  properly  it  is  also  too  weak  to  fill 
itself,  p.  54. 

In  adult  and  later  life  increasing  rigidity  of  the  cardiac 
tissues  increases  the  liability  to  overfilling  and  to  the  occurrence 
of  anginal  pain,  pp.  82,  148. 

Also  as  regards  sudden  death  from  asystole. 

For  the  above  reason  this  is  very  rare  in  the  myocardial 
weakness  of  early  life  ;  but  in  later  life  the  liability  to  sudden 
death  in  myocardial  disease  increases  as  age  advances,  p.  54. 

Heart  Failure  without  Enlargement  in  Adolescence 

Clinical  Features  of  heart  failure  without  enlargement 
in  distensible  hearts — namely,  in  heart  failure  with  small  heart. 

As  has  already  been  pointed  out,  where  the  heait  is 
distensible  (as  it  is  in  adolescence)  severe  muscular  failure 
is  accompanied  clinically  by  a  diminution  in  the  size  of  the 
heart. 

General  Symptoms. 

Extreme  weakness.  Faintness  on  the  shghtest  exertion 
—  sometimes  even  on  raising  the  arm  from  the  side. 


568  SUMMARY 

Pulse  very  weak  and  small,  pp.  35,  56, 59,  95. 

Special  character  of  pulse  in  myocardial  weakness. 

A  high  tension  pulse  of  very  low^  pressure  and  very  small 
volume,  p.  59. 

Compensatory  contraction  of  the  peripheral  arterioles  in 
extreme  heart  weakness,  p.  59. 

Illustration :  the  pulse  characteristic  of  severe  enteric 
fever,  p.  59. 

Very  weak  or  absent  impulse  in  jugular  bulb,  pp.  97,  (98). 

Emptiness  of  the  neck  veins,  p.  61. 

In  the  distensible  heart  of  adolescence,  full  reliance  can 
be  placed  on  the  diminution  in  the  size  of  the  heart  itself  and 
in  the  evidences  of  compensatory  diminution  in  the  blood 
volume  given  by  the  rise  of  the  diaphragm  and  diminution 
in  the  size  of  the  absolute  liver  dullness,  p.  56. 

Physical  Signs  relating  to  the  heart  itself.  Cardiac 
impulse — weak  or  absent,  pp.  56,  96. 

Evidence  of  diminution  in  the  size  of  the  heart.  Cardiac 
dullness  small  or  absent,  pp.  56,  60,  96,  187. 

Diminution  not  due  to  increase  in  size  of  lungs,  as  is  shown 
by  diminution  in  their  size,  pp.  57,  (98). 

Complete  disappearance  of  dullness,  when  it  occurs,  is 
probably  partly  due  to  falhng  backwards  of  the  small  and 
badly  filled  heart,  p.  56. 

Cases  showing  extreme  smallness  or  absence  of  cardiac 
dullness,  p.  (65),  (68),  and  (118). 

A  lessening  in  the  size  of  a  dilated  heart  may  be  the  sign 
of  the  onset  of  myocardial  weakness,  p.  (316). 

Feebleness  of  heart  sounds,  pp.  60,  96. 

Loudness  ■  of  pulmonary  second  sound  of  importance, 
p.  96. 

Evidences  of  a  compensatoey  diminution  in  the  volume 
OF  BLOOD  in  circulation,  p.  55,  577. 

Diminution  in  the  volume  of  the  thoracic  contents 
from  underfilling  of  the  lungs  and  gi'eat  vessels  with  blood, 
pp.  57,  163. 

Diaphragm  raised,  pp.  57,  163, 180.  Shown  by  high  gastric 
resonance,  pp.  57,  164. 

Upper  level  of  liver  dullness  high,  pp.  57,  165. 


HEAKT  FAILURE  WITHOUT  ENLARGEMENT       569 

Signs  that  the  Hver  is  underfilled  with  blood,  pp.  187,  191. 

Diminution  in  its  area  of  absolute  dullness,  pp.  95,  &c. 

Diagnostic  value  of  high  diaphragm  and  small  liver  dullness 
in  heart  weakness,  pp.  56,  72,  (97),  (195),  (32G). 

Diminution  in  the  absolute  dullness  of  the  liver  due  to 
causes  other  than  heart  weakness,  p.  152,  202. 

Disappearance  of  these  signs  as  the  heart  regains  its 
muscular  strength,  pp.  (196),  &c. 

Heart  Failure  without  Enlargement  in  Adult  Life 

Clinical  Features  of  heart  failure,  without  enlargement, 
in  the  moderately  distensible  heart  of  adult  life. 

In  adult  hfe  the  lessened  distensibility  of  the  heart  lessens 
the  amount  of  its  diminution  in  size  when  very  weak,  and  also 
lessens  the  extreme  movements  of  the  diaphragm,  which  are 
noticeable  with  the  softer  fibrous  tissues  of  early  life,  pp.  72,  79. 

SjToaptoms  of  general  weakness,  smaUness  of  pulse  and 
feebleness  of  heart's  impulse  and  heart  sounds  are  of  value  as 
in  adolescence,  p.  91. 

With  the  lessened  possibility  of  change  in  the  size  of  the 
heart,  more  dependence  is  placed  upon  the  available  signs  of 
compensatory  diminution  in  the  blood  volume,  pp.  51,  61,  94. 

Of  these  the  most  reliable  are  : — 

Rise  in  the  level  of  the  gastric  resonance. 

Evidences  of  lessened  volume  of  the  thoracic  contents  given 
by  hollowing  of  the  supra-clavicular  fossse  (where  the  dia- 
phragm is  too  rigid  to  rise  adequately),  pp.  94,  134,  187. 

Evidences  of  weak  and  ineffective  action  of  the  right 
ventricle  given  by  feebleness  and  smaUness  or  even  absence 
of  the  jugular  bulb  pulsation,  pp.  (98),  133. 

Emptiness  of  the  veins  of  the  neck  may  be  of  value — 
especially  in  cases  where  fullness  might  be  expected,  pp.  98, 
(133). 

Diminution  in  the  size  of  the  absolute  liver  dullness.  The 
greater  the  distensibility  the  more  nearly  will  the  clinical 
features  approximate  to  those  of  adolfscence.  This  is  also 
true  of  heart  failure  in  later  hfe,  p.  195. 

In  a  moderatelj^  distensible  heart,  failure  due  to  myocardial 
weakness   can    often    be    diagnosed    by  the   absence  of  the 


570  SUMMARY 

dilatation  and  venous  fullness  or  of  right  ventricular  overaction, 
under  circumstances  calculated  to  produce  signs  of  right 
ventricular  overstrain— such,  for  instance,  as  pneumonia,  pp. 
(97),  (105),  or  in  valvular  disease,  pp.  62,  64. 

Assistance  may  be  given  in  the  diagnosis  of  myocardial 
weakness  by  the  presence  of  pain  in  the  calves  on  exertion 
from  faultj^  blood  supply  to   the  muscles,  pp.  92,  467,  (470). 

Also  coldness  on  exertion  from  faulty  blood  supply,  pp.  (365), 
472,  (473),  (475). 

Enlakgement  of  a  Small  Heart  a  Sign  of  Eeturning 

Strength 

From  what  has  just  been  said  it  follows  that : — 

Increase  in  the  size  of  a  heart  that  has  diminished  in  size, 
owing  to  myocardial  weakness,  will  be  a  sign  of  returning 
strength,  or  in  a  weak  heart,  dilatation  may  be  a  sign  of 
returning  strength,  p.  63. 

niustrative  cases,  pp.  (64),  (294),  (304). 

Similarly,  the  return  of  cardiac  strength  may  be  measm-ed 
by  the  increase  in  the  size  of  the  absolute  liver  dullness,  p.  64. 

Illustrative  cases,  pp.  (66),  (195),  &c. 

Also  by  the  return  of  the  diaphragm  (as  shown  by  the 
level  of  the  gastric  resonance)  towards  its  normal  position, 
pp.  (118),  (196),  &c. 

Return  of  strength  will  also  be  shown  by  lessening  of  the 
upward  dilatation  due  to  recumbency,  p.  315. 

Also,  on  the  gradual  retm-n  of  strength  in  a  distensible 
heart,  a  point  is  usually  reached  when  the  strength  of  the 
stronger  part  of  the  right  ventricle  exceeds  that  of  the  weak 
part  of  the  anterior  waU  ;  and  even  though  the  patient  be 
confined  to  bed,  upward  dilatation  with  abnormal  pulsation 
occm-s,  fig.  46,  p.  197. 

Upward  dilatation  of  the  right  ventiicle  a  sign  of  returning 
strength  after  myocardial  weakness. 

Illustrative  cases,  pp.  (102),  (294),  (304),  &c. 

Thus  the  physical  signs  of  the  return  of  strength  in  a  weak 
heart  are  the  same  as  those  of  heart  failure  in  a  strong  heart, 
pp.  63,  71. 

For  other  cases,  see  pp.  (64),  (100),  (157),  (182),  (196),  (316). 


HEART  FAILURE  IN  LATER  LIFE  571 

A  Summary  and  Index  of  Arguments  and  Facts  brought 

FORWARD     IN     CONNECTION    WITH    EaRLY     DIAGNOSIS     OF 

Heart  Failure  in  Later  Life 

The  early  diagnosis  of  heart  failure  as  age  advances  becomes 
more  difficult  than  is  the  case  earlier  in  life,  for  the  following 
reasons  : — 

I.  Owing  to  the  increasing  rigidity  of  the  cardiac  and 
pericardial  tissues  in  later  life,  changes  in  the  size  of  the  heart, 
indicative  of  heart  failure,  take  place  less  readily  and  in  extreme 
cases  not  at  all,  pp.  72,  79. 

(a)  Dilatation,  when  it  does  occur,  will  be  less  in  amount 

for  any  definite  degree  of  overstrain,  p.  87. 

(b)  There  will  be  a  larger  proportion  of  cases  where  the 

diagnosis  will  be  rendered  more  difficult  by  the  fact 
that    cardiac    failure    is    not    accompanied    by    any 
clinical  evidences  of  dilatation,  pp.  79,  87. 
Early  diagnosis  of  failure  in  such  cases,  p.  90. 

(c)  There  will  be  a  lessened  likelihood,  in  the  case  of  myo- 

cardial weakness,  that  extreme  heart  failure  will  show 
itself  by  diminution  in  the  size  of  the  heart,  p.  80. 

Estimation  of  the  degree  of  rigidity  possessed  by  the  heart 
wall  is  of  great  importance  in  later  life,  but  of  considerable 
difficulty,  p.  147. 

In  the  absence  of  signs  due  to  changes  in  the  size  of  the 
heart,  increased  dependence  has  to  be  placed  upon  the  less 
certain  signs  given  by  changes  in  the  volume  of  blood  in  circu- 
lation, and  especially  upon  the  evidences  of  fullness  or  emptiness 
of  the  auriculo-venous  reservoir  and  of  the  lungs. 

II.  The  increasing  rigidity  of  the  fibrous  tissues  of  the 
body  generally  will  interfere — 

(1)  With  the  physical   signs  w^hereby  overfullness  of   the 

auriculo-venous  reservoir,  and  of  the  lungs,  manifests 
itself  in  cases  of  cardiac  failure  with  a  moderately 
strong  heart ;  and  also — 

(2)  With  the  physical  signs,  whereby  compensatory  dimi- 

nution of  the  blood  volume  manifests  itself  in  cases  of 
very  considerable  cardiac  weakness,  p.  72. 
(a)  Alterations  in  the'  level  of  the  diaphragm  will  take 
place  less  readily,'^ p.  72. 


572  SUMMARY 

{b)  Fullness  or  emptiness  of  the  supra-clavicular  fossae,  as 
evidence  of  increased  or  diminished  volume  of  the 
intrathoracic  contents,  while  not  being  so  greatly  inter- 
fered with  as  is  the  case  with  changes  in  the  average 
level  of  the  diaphragm,  will,  nevertheless,  be  lessened 
by  increasing  rigidity  of  the  fibrous  tissues, 
(c)  Changes  in  the  size  and  flaccidity  of  the  liver  will  be 
less  marked,  and  less  extreme  variations  in  the  size 
of  its  absolute  dullness  may  be  expected. 
III.  There  are  difficulties  in  appraising  the  true  value  of 
the  radial  pulse  and  of  the  blood  pressure  as  estimated  by  the 
sphygmomanometer,  owing  to  the  frequency  of  abnormalities 
of  the  blood  pressure  in  later  life,  p.  143. 

Difficulties  consequently  occur  in  estimating  what  may  be 
called  the  internal  work  that  the  heart  is  doing,  p.  73. 

There  is  need  for  very  carefully  estimating  the  bearing  of 
such  high  arterial  resistance,  as  may  be  present,  upon  the 
heart's  action,  p.  74. 

1.  Increased  arterial  resistance  may  be  pathological,  due 
to  arterial  disease  or  spasm,  and  the  rise  in  blood  pressure 
so  caused  may  be  throwing  an  extra  burden  on  the  heart, 
p.   143. 

(a)  Owing,  however,  to  abnormal  rigidity  of  the  heart  wall 

no  evidence  of    this  fact  may  be  given    by  cardiac 
dilatation. 

(b)  Owing  to  myocardial  weakness  no  evidence  may  be 

given   by  increased  vigour  of  cardiac  action  of  the 
extra  burden  that  is  being  thrown  upon  the  heart. 

2.  Increased  arterial  resistance  may  be  compensatory  in 
nature,  because  the  heart  is  better  nourished  by  a  high  than 
by  a  low  blood  pressure  (owing  to  blocking  of  the  coronary 
arteries  or  other  cause),  p.  144. 

3.  High  blood  pressure,  due  to  increased  arterial  resistance, 
may  be  (owing  to  the  presence  of  myocardial  weakness)  less 
than  is  necessary  for  adequate  nourishment  of  the  heart. 
In  such  a  case  as  this  a  rise  in  the  already  high  blood  pressure 
accompanies  the  return  of  the  heart  to  a  more  normal  mode 
of  working,  p.  146. 

Complexity  of  the  inter-relationship  in  later  life  between 


HEART  FAILURE  IN  LATER  LIFE  573 

arterial  resistance — the  amount  oi  Avork  done  by  the  heart 
and  the  distensibiUty  of  the  heart  wall,  p.  142. 

The  radial  pulse.     Its  diagnostic  value,  p.  143. 

Sphygmo-oscillometer.  Its  great  value  as  showing  the 
type  of  high  blood- pressure  present  in  any  case,  p.  145. 

Compensatory  and  non-compensatory  high  blood  pressure 
show  a  different  type  of  oscillation,  p.  145. 

In  heart  failure  with  high  blood  pressm-e,  a  further  rise 
may  sometimes  be  followed  by  improvement  in  the  heart,  p.  146. 

Abnormality  of  the  blood  pressure  may  be  due  to  a  lessening 
of  the  elasticity  of  the  first  part  of  the  aorta,  p.  (109). 

lY.  Difiiculties  associated  with  myocardial  weakness  due 
to  interference  with  the  blood  supply  by  arterial  disease 
affecting  the  coronary  arteries,  p.  75. 

The  myocardial  weakness  of  later  life  is  much  more  difficult 
to  recognise  than  that  of  adolescence  and  early  adult  life. 

1.  The  rigidity  of  the  cardiac  tissues  in  later  life  lessens 
the  likelihood  of  myocardial  weakness  being  accompanied  by 
recognisible  reduction  in  the  size  of  the  heart. 

2.  The  increased  fibrous  strength  of  the  heart  waU  which 
is  apt  to  characterise  later  hfe  is  very  apt  to  be  mistaken  for 
muscular  strength,  pp.  34,  150. 

A  heart  which  does  not  dilate  when  subject  to  overstrain 
is  not  infrequently  (in  later  Hfe)  weaker  muscularly  than  a 
heart  which  does  dilate. 

Need  for  distinguishing  clinically  between  the  fibrous 
strength  of  the  heart  wall  and  its  muscular  power,  and  deciding 
in  a  case  of  heart  failure  without  enlargement  whether  its 
non-dilatation  is  due  to  rigid  walls  or  weak  muscle,  p.  73. 

3.  Difficulty  in  estimating  the  amount  of  power  developed 
b}^  the  heart  muscle  in  later  hfe  (easy  in  early  hfe),  p.  142. 

4.  Myocardial  weakness  due  to  disease  of  the  coronary 
arteries  is  apt  to  be  much  more  insidious  in  its  onset  than  that 
of  adolescence  and  early  adult  life,  which  is  usually  infective 
m  character  and  has  some  obvious  cause,  p.  153. 

5.  Cardiac  weakness  of  this  type  is  apt  to  increase  so 
gradually  that  compensatory  changes  in  the  chculation  and 
the  patient's  habits  may  prevent  the  appearance  of  any 
obvious  symptoms  in  its  earlier  stages,  p.  75. 


574  SUMMARY 

6.  Disease  onhe  coronaiy  arteries  often  interferes  with  the 
nutrition  of  only  a  portion  of  the  heart  muscle,  and  not  the 
whole  as  in  infective  myocardial  weakness,  p.  75. 

Difficulties  arise  when  one  ventricle  is  strong  and  the  other 
weak,  p.  153. 

Need  for  distinguishing  between  the  phenomena  due  to 
weakness  of  the  right  ventricle  and  those  due  to  the  left, 
p.  154. 

Dyspnoea  a  symptom  of  right  ventricle  weakness,  pp.  (154), 
(156). 

Faintness  and  ^veariness  a  sign  of  weak  left  ventricle,  pp.  121, 
(124),  154. 

Leg  pains  on  exertion  a  sign  of  weak  left  ventricle,  pp.  92, 
467,  469. 

Coldness  on  exertion  a  sign  of  myocardial  weakness  of 
left  ventricle,  p.  (365),  471. 

Signs  w^hen  left  ventricle  strong  and  right  one  w^eak, 
pp.  (109),  (154),  (156). 

Signs  when  right  ventricle  strong  and  left  one  weak, 
p.  (107). 

Strong  collapsing  radial  pulse  in  severe  fatty  degeneration 
of  right  ventricle  with  strong  left  ventricle,  p.  154. 

7.  Difficulties  associated  with  the  diagnosis  of  the  onset 
of  myocardial  weakness  in  general,  or  with  the  return  of 
cardiac  vigour  on  its  subsidence. 

The  physical  signs  of  failm-e  in  a  muscularly  weak  heart  are 
the  reverse  of  those  in  a  stronger  one,  p.  71. 

In  a  moderately  distensible  heart  in  adult  and  later  hfe 
dangerous  heart  weakness  may  be  shown  by  the  absence  of  the 
ordinary  signs  of  heart  failure,  p.  71. 

Cases  of  pneumonia  illustrating  this,  pp.  (97),  (106). 

In  a  moderately  strong  heart  which  is  showing  signs  of 
failure  with  enlargement  and  venous  plethora,  the  signs  of 
the  onset  of  myocardial  weakness  are,  in  many  respects,  the 
same  as  those  of  retm-ning  strength,  p.  llO. 

Illustrative  case.  Lessened  right  ventricular  pulsation :  at 
one  time  showing  improvement,  at  another  dangerous  w^eak- 
ness  in  the  same  patient,  pp.  (106),  (141). 

Diminution  in    the  size  of  a  liver    enlarged  by  tricuspid 


HEART  FAILURE  IN  LATER  LIFE  575 

regurgitation,  a  sign  of  deterioration  and  not  improvement, 
pp.  (63),  (110). 

The  signs  of  the  retmii  of  strength  after  myocardial 
weakness  in  a  weak  heart  may  be  the  same  as  those  of  the 
onset  of  heart  failure  in  a  moderately  strong  heart. 

Summary  of  phenomena,  which  may  indicate  either 
increasing  or  decreasing  weakness  of  the  heart,  p.  160. 

V.  Difficulties  arising  from  the  fact  that  greater  dependence 
has  to  be  placed  upon  general  symptoms  of  heart  failure, 
and  the  fact  that  they  are  often  misleading. 
Breathlessness,  pp.  92,  113. 

Tachycardia  in  its  relation  to  dyspnoea,  p.  113. 
Importance   of    breathlessness   as   showing   a    muscularly 
weak  right  ventricle,  pp.  93,  (155),  (156). 
Palpitation,  p.  114. 

Fmictional  palpitation  and  irregularity  simulating  organic 

disease,  p.  (115). 
Reflex  palpitation  simulating  cardiac  overstrain,  p.  (115). 
Colon  dyspepsia  a  cause  of  palpitation,  p.  (116). 
Nocturnal  attacks  of  palpitation  suggest  a  reflex  colon 

origin,  p.  (116). 
Palpitation  as  a  cardiac  habit  after  recovery  from  severe 

asthenia,  p.  (117). 
Habit   palpitation  after   influenza   and   after   diphtheritic 
cardiac  weakness,  p.  (119). 
Faintness,  pp.  92,  (121). 

Fainting  and  asthenia  of  labyrinthine  origin  liable  to  be 
mistaken  for  a  sign  of  dangerous  heart  weakness,  pp.  122, 
123. 
Faintness  of  cardiac  origin  diagnosed  as  of  gastric  origin, 

p.  (124). 
Danger  of  fatal  syncope  in  cardiac  asthenia  from  micturition 

in  erect  attitude,  p.  126. 
Sudden  death  when  right  ventricle  is  weak  and  left  one 
strong — probably  due  to  fainting  from  deficient  supply  of 
blood  to  the  left  ventricle,  p.  125. 
Sudden  death  when  right  ventricle  stronger  than  the  left 
apt  to  be  due  to  asystole  from  an  overfilling  of  the 
weak  left  ventricle. 


576  SUMMARY 

Anginal  pain,  p.  126. 

Liability  of  mistaking  false  angina  for  true. 

Vasomotor   angina    of    reflex    origin   in  colon  dyspepsia, 
pp.  (127),  (130). 

Value  of  nitroglycerine  in  reflex  angina,  pp.  (127),  (130). 

Anginal  pain  produced  by  palpation  of  an  irritable  colon, 
p.  129. 

Nocturnal  occurrence  of  attacks  suggests  colon  origin,  p.  131. 

Anginal  pain  not   likely  to  occur  in  early  life   because  of 
compensatory  underfilling  of  the  ventricle,  p.  53. 

Anginal  pain  more  likely  to  occur  the  greater  the  relative 
rigidity  of  the  heart,  because  the  presence  of  mechanical 
elastic  recoil  interferes   with  the   compensatory   under- 
filling of   the  heart,  pp.  82,  148. 
Leg   pains    and   intermittent   claudication    a    sign    of    myo- 
cardial weakness,  pp.  92,  469. 

Summary  of  Evidences  op  Heart  Failure  in  Later  Life 

Clinically,  in  the  diagnosis  of  heart  failure  with  weak 
heart  in  later  life,  reliance  must  be  placed  upon  the  symptom 
of  breathlessness  in  the  first  place. 

Faintness  or  vertigo,  if  of  cardiac  origin,  is  of  serious 
import,  p.  121. 

A  very  weak  or  low  pressure  pulse  is  important  evidence. 
If  normal  or  strong  its  meaning  must  be  carefully  analysed, 
p.  143. 

Weak  or  absent  jugular  bulb  pulsation  is  of  great  clinical 
value.  A  strong  and  full  jugular  pulse  without  any  cardiac 
dilatation  suggests  undue  cardiac  rigidity,  p.  134. 

The  venous  phenomena  are  of  much  importance  (see  p.  132, 
and  table,  p.  137). 

Amongst  physical  signs,  most  dependence  must  be  placed 
upon  those  of  a  compensatory  diminution  in  the  volume 
of  blood  hi  circulation — especially 

(1)  High  gastric  resonance,  56,  163,  185. 
^  (2)  Hollo wness  of  supra- clavicular  foss^  and  emptiness  of 
the  neck  veins,  p.  134. 

(3)  Diminution    of    the     absolute    liver     dullness   (when 


DIMINUTION  OF  BLOOD  VOLUME  577 

present)  suggesting  altered  conductivity  to  percussion 
vibrations  by  lessened  tension  of  its  tissue  from  underfilling 
with  blood,  p.  191. 

4.  Weak  heart  sounds  and  impulse  are  important,  if 
not  explicable  by  changes  in  lung  or  thoracic  wall,  p.  152. 

As  a  result  of  what  has  been  said  as  to  the  occurrence  of 
heart  failure  without  enlargement  in  a  strong  but  relatively 
rigid  heart,  and  also  in  a  weak  and  rigid  heart,  it  follows  that 
it  is  possible  to  have  a  case  of  heart  failure  where  the  size  and 
mode  of  action  of  the  heart  appear  normal  in  every  respect, 
p.  148. 

Such  a  possible  case  analysed,  p.  149. 

Difficulties  in  diagnoses  in  later  hfe.  Summary  of  opposing 
and  apparently  contradictory  statements,  p.  160. 

A  Summary  and  Index  of  Arguments  and  Facts  brought 

FORWARD     IN     CONNECTION     WITH     COMPENSATORY     DIMI- 
NUTION OF  THE  Blood  Volume 

In  cases  where  the  amount  of  food  is  limited,  as  in  the 
treatment  of  gastric  ulcer,  or  where  the  absorption  of  nourish- 
ment is  interfered  with,  as  in  enteric  fever,  a  progressive 
diminution  in  the  volume  of  the  thoracic  contents  is  noticeable, 
as  CAddenced  by  a  rise  in  the  diaphragm,  pp.  168, 178. 

The  only  variable  substance  in  the  thorax  is  the  blood 
contained  in  the  heart  and  the  blood-vessels — especially  those 
of  the  lungs,  p.  179. 

Therefore  a  diminution  in  the  bulk  of  the  thoracic  contents 
must  mean  a  diminution  in  the  amount  of  blood  contained 
in  it. 

Further,  on  post-mortem  examination  of,  for  instance,  a 
case  of  enteric  fever  dying  of  asthenia  from  non-absorption 
of  food,  the  diaphragm  is  found  to  be  abnormally  high  and 
'  the  organs  of  the  body  extraordinarily  dry  and  bloodless,' 
p.  168. 

These  and  similar  observations  point  to  the  fact  that  where 
there  are  insufficient  materials  available  for  the  formation  of 
the  normal  amount  of  blood  of  the  proper  specific  gravity,  an 
abnormally  small  amount  of  blood  of  a  good  specific  gravity 

2p 


578  SUMMAKY 

is  maintained  in  circulation  rather  than  a  nearly  normal 
amount  of  an  abnormally  low  specific  gravity,  p.  180. 

In  other  words  :  there  is  clinical  evidence  that  the  total 
volume  of  the  blood  in  circulation  is  reduced  when  the  essential 
constituents  of  the  blood  fall  below  a  certain  definite  minimum. 

In  the  case  of  the  specific  gravity,  observation  would 
probably  determine  what  the  minimum  was,  below  which  the 
specific  gravity  of  the  blood  was  not  allowed  to  fall,  p.  180. 

This  is  a  fruitful  field  for  research. 

This  compensatory  diminution  in  the  volume  of  the  blood 
can  be  observed  clinically  under  the  following  conditions  : — 

1.  Limitation  of  ordinary  food,  as  in  the  treatment  of 
gastric  ulcer,  pp.  169,  194,  204. 

Starvation  due  to  disease,  e.g.  enteric  fever,  p.  168. 
Mahiutrition  from  any  cause,  e.g.  anaemia,  pp.  176,  203, 

2.  Limitation  of  water. 

In  cases  of  diarrhoea  and  vomiting,  p.  203. 

3.  Loss  of  blood  from  severe  haemorrhage,  pp.  175,  203. 

4.  Deficiency  of  thyroid  secretion,  pp.  178,  195,  206. 

5.  In  cases  of  neurasthenia  from  the  deficiency  of  some 
unlmown  material  necessary  for  the  nutrition  of  the  nervous 
system,  pp.  177,  195,  207. 

These  observations  seem  to  show  that  there  are  certain 
essential  constituents  of  the  blood  and  that  each  has  a  minimal 
percentage  below  which  it  is  not  allowed  to  fall.  In  the  case 
of  a  great  deficiency,  the  total  volume  of  blood  must  be 
lessened  in  order  that  an  adequate  percentage  composition 
may  be  maintained  in  spite  of  the  inadequate  supply  of  the 
particular  substance. 

COMPENSATOEY   DIMINUTION    IN    THE    BlOOD    VoLUME    DUE  TO 

Cardiac  Inefficiency 

Not  only  is  the  total  volume  of  the  blood  diminished  when 
materials  for  its  formation  are  deficient,  but  the  amount  of 
blood  in  circulation  is  compensatorily  diminished  when  the 
strength  of  the  heart  is  insufiicient  for  the  circulation  of  the 


DIMINUTION  OF  BLOOD  VOLUME  579 

normal  amount.  Observation  of  cases  of  cardiac  weakness 
gives  precisely  the  same  signs  of  deficiency  in  the  blood  volume 
as  those  just  described,  pp.  53,  180,  185. 

In  cardiac  weakness,  the  compensatory  emptiness  of  the 
blood-vessels  does  not  necessarily  imply  deficiency  of  the  toial 
amount  in  the  body. 

There  are  evidently  reserves  which  can  be  drawn  upon  if 
desired.     Case  proving  this,  pp.  (141),  186. 

The  rationale  of  compensatory  diminution  in  the  amount 
of  the  circulating  blood  in  heart  w^eakness  is  clear.  The  work 
the  heart  has  to  do  is  cut  down  proportionally  to  its  power  of 
doing  it.  The  heart's  load  is  made  proportional  to  its  strength, 
pp.  50,  55,  180,  186. 

The  mechanism  whereby  this  is  brought  about  is  simple. 
In  the  distensible  heart  of  adolescence  (which  depends  on  its 
muscular  expansion  alone  for  its  power  of  filling  itself)  the 
same  weakness  w^hich  interferes  with  the  emptying  of  the  heart 
will  interfere  equally  with  its  power  of  filling  itself,  p.  52. 

In  the  less  distensible  heart,  which  possesses  mechanical 
elastic  recoil,  although  the  compensatory  diminution  in  the 
filling  may  be  less  complete,  it  nevertheless  takes  place,  for 
the  amount  of  elastic  recoil  is  directly  dependent  on  the  vigour 
of  the  preceding  contraction,  pp.  53,  79. 

Evidences  of  a  diminution  in  the  volume  of  the  blood  are 
of  the  utmost  value  in  the  diagnosis  of  myocardial  weakness, 
and  especially  so  in  adults  and  in  later  life  where,  owing  to 
increasing  rigidity  of  the  heart,  less  dependence  than  in  early 
life  can  be  placed  upon  the  condition  of  the  heart  itself,  p.  186. 

The  main  clinical  signs  of  compensatory  diminution  of  the 
blood  volume  depend  upon  the  lessened  distension  with  blood 
of  the  more  elastic  and  vascular  of  the  viscera  which  are 
readily  studied  clinically. 

Of  these  the  lungs,  the  heart,  and  the  liver  are  of  most 
importance,  p.  187. 

1.  Diminished  distension  of  the  lungs  with  blood  (in 
conjunction  with  a  similar  condition  of  the  heart  and  great 


580  SUMMARY 

veins)  causes  what  is,  in  effect,  a  negative  pressure  within 
the  thorax,  and  this  shows  itself  cUnically  by  changes  in  the 
less  rigid  portions  of  its  walls — that  is  by — 

(1)  A  rise  in  the  level  of  its  floor — namely,  the  diaphragm, 
pp.  57,  180  ;  and — 

(2)  By  a  sinking-in  of  the  soft  tissues  which  fill  in  the  space 
which  is  enclosed  by  the  first  rib  on  either  side — namely,  the 
tissues  which  occupy  the  supra-clavicular  fossae,  pp.  94, 134, 139. 

(1)  A  rise  in  the  level  of  the  diaphragm. 

This  may  be  measured  clinically  by  noting — 

(a)  The  level  of  the  gastric  resonance  (normally,  the  sixth 
interspace)  as  marking  its  level  on  the  left  side,  pp.  57,  164, 
(171),  &c. 

{h)  The  upper  level  of  the  liver  dullness  as  marking  its  level 
on  the  right  side,  p.  165. 

(c)  The  lower  level  of  the  liver  dullness  may  also  rise  owing 
to  the  organ  being  drawn  up  under  the  highly  arched  dia- 
phragm. This  change  is  less  certain  and  of  less  diagnostic 
value  than  the  two  above  mentioned  and  need  not  be  further 
dealt  with. 

In  the  first  two  or  three  decades  of  life  this  alteration  in 
the  diaphragm  takes  place  readily  owing  to  the  softness  of 
the  fibrous  tissues.  It  constitutes  a  sufficient  guide  to  the 
amount  of  blood  in  circulation  in  the  thoracic  viscera. 

In  heart  weakness  the  level  of  the  diaphi-agm  must  be 
carefully  watched  from  day  to  day.  It  is  of  much  diagnostic 
value.  The  gastric  resonance  sometimes  reaches  up  to  the 
fourth  rib,  pp.  (68),  (118),  and  (182). 

The  changes  in  level  of  the  liver  dullness  are  apt  to  be 
interfered  with  by  the  inertia  of  the  liver  ;  but,  nevertheless,  in 
young  subjects  with  extreme  heart  wealmess  the  upper  border  of 
its  relative  dullness  may  rise  as  high  as  the  third  rib,  p.  (182). 

In  adult  and  later  life,  changes  in  the  level  of  the 
diaphragm  are  less  extreme,  owing  to  the  increasing  rigidity 
of  the  fibrous  tissues,  pp.  72,  94. 

Changes  in  the  upper  level  of  the  liver  dullness  are  in  later 
life  too  slight  to  be  of  clinical  value  owing  to  this  cause  ;  but 
changes  in  the  level  of  the  gastric  resonance  are,  as  a  rule, 
still  of  diagnostic  importance,  p.  94. 


DDITNUTION  OF  BLOOD  VOLUME  581 

(2)  Eecession  of  the  tissues  in  the  supra-ckivicular  fossa) 
as  a  sign  of  diminished  circulation  in  the  thoracic  viscera. 

"While  the  fibrous  tissues  still  remam  distensible,  the 
changes  in  the  diaphragm  are  adequate  to  compensate  for 
any  degree  of  diminution  in  th(^  bulk  of  the  thoracic  con- 
tents, therefore  no  hollowing  of  the  supra-clavicular  fossae  is 
noticeable. 

In  later  life,  however,  the  greater  rigidity  of  the  diaphragm 
makes  it  less  able  to  compensate  by  its  mobility  for  alterations 
in  the  size  of  the  thoracic  viscera.  Under  these  circumstances 
sufficient  negative  pressm'e  may  be  developed  by  compensatory 
diminution  of  the  blood  volume  to  cause  hollowing  of  the  supra- 
clavicular fossae.  Hollowing  of  the  supra-clavicular  fossae  a 
valuable  sign  of  heart  faihu'e  in  later  life,  pp.  94,  134,  139. 

2.  Diminution  in  the  size  of  the  heart  a  sign  oi  compensatory 
diminution  in  the  blood  volume,  p.  188. 

This  diminution  in  the  size  of  the  heart  as  observed  clinically 
is  of  far  greater  diagnostic  importance  where  the  lessened 
blood  volume  is  due  to  cardiac  weakness  than  when  due  to 
lessened  volume  from  nutritional  and  allied  causes.  It  is 
sometimes  extreme  in  great  myocardial  weakness,  causing, 
even,  complete  disappearance  of  both  absolute  and  relative 
cardiac  dullness,  pp.  54,  (68),  and  (118). 

This  is  a  sign  that  is  most  evident  when  the  cardiac  tissues 
are  soft  in  the  first  two  or  three  decades  of  life. 

In  adult  life  the  increasing  relative  rigidity  of  the  cardiac 
tissues,  while  not  interfering  very  greatly  with  compensatory 
diminution  of  the  blood  volume  in  cardiac  weakness,  does 
interfere  with  the  diminution  in  the  size  of  the  heart,  pp. 
81,  82. 

In  later  life  the  relative  rigidity  of  the  heart  may  entu'ely 
prevent  any  observable  diminution  in  its  size,  even  though 
there  is  considerable  compensatory  diminution  in  the  volume 
of  the  blood  which  it  is  able  to  keep  in  circulation. 

3.  Diminished  distension  of  the  hver  with  blood  causes 
certain  changes  which  are  observable  chnically  and  are  of 
gi-eat  diagnostic  value  in  determining  the  amount  of  blood 
in  active  circulation,  p.  185. 

These  changes  show  clinically  by  a  diminution  in  the  area 


582  SUMMARY 

of  the  liver  dullness  involving  both  its  relative  and  absolute 
dullness. 

The  changes  in  absolute  dullness  are  more  marked  than 
those  in  the  relative  dullness  and  are  of  much  greater 
diagnostic  value. 

Diminution  in  the  area  of  liver  dullness  from  this  cause  is 
brought  about — 

(1)  By  an  actual  diminution  in  the  size  of  the  liver  owing 
to  its  lessened  distension  with  blood,  pp.  188,  189. 

(2)  The  insufficient  distension  causes  the  liver  to  be  more 
flaccid  than  normal,  and  its  thin  edge  is  apt  to  fall  back  and 
allow  the  approach  of  the  resonant  intestines  to  the  ribs. 
Case  tending  to  prove  the  flaccidity  of  the  liver  in  a  case  of 
voluntary  starvation  for  gastric  ulcer,  pp.  190,  (205). 

(3)  Neither  of  these  explanations  is  adequate  to  explain 
the  more  extreme  cases  of  absence  of  absolute  liver  dullness 
which  are  met  with  clinically,  p.  191. 

It  is  certain  that  over- distension  of  the  liver  tissue  with 
blood,  in  chronic  venous  congestion,  deprives  the  liver  tissue 
of  its  power  of  masking  the  resonance  of  the  underlying 
intestines  and  thus  increases  its  conductivity  to  percussion 
vibrations,  p.  24. 

It  seems  probable  that  the  lessened  tension  of  its  tissue 
which  results  from  imderfiJHng  with  blood  also  has  this  power 
of  increasing  its  power  of  conducting  percussion  vibrations  to 
and  from  the  underlying  resonant  intestines. 

Clinically,  the  absolute  dullness  of  the  liver  varies  in  extent 
in  such  a  way  as  to  show  that  the  degree  of  its  diminution  is 
an  absolutely  rehable  guide  to  the  degi-ee  to  which  the  liver 
tissue  is  relaxed  from  underfilling  with  blood,  p.  (195). 

These  changes  which  indicate  the  degree  to  which  the  blood 
volume  is  being  compensatorily  diminished  are  of  great  clinical 
value  in  estimating  the  effect  of  starvation  or  rectal  feeding 
on  a  patient.  Thus  showing  the  safety  or  otherwise  of  its 
continuance,  p.  205. 

But  they  are  of  much  greater  clinical  value  as  showing 
the  degree  in  which  the  volume  of  blood  in  circulation  in 
the  liver  is  compensatorily  lessened  when  there  is  muscular 
weakness  of  the  heart,  p.  185. 


DIMINUTION  OF  BLOOD  VOLUME  583 

In  cases  of  increasing  cardiac  weakness,  the  diminution 
of  the  absolute  Hver  dullness  is  noticeable  from  day  to  day  as 
the  heart  gets  weaker,  and  in  the  same  way  its  return  towards 
the  normal  size  is  an  accurate  measure  of  the  return  of  the 
heart's  strength,  pp.  (195)  to  (199). 

Although  this  does  not  always  take  place,  the  size  of  the 
absolute  liver  dullness  does  as  a  rule  give  very  valuable  indica- 
tions as  to  the  amount  of  blood  the  heart  is  able  to  keep  in 
circulation. 

The  regular  way  in  which  variations  in  the  area  of  absolute 
liver  dullness  respond  to  variations  in  the  heart's  activity 
suggests  that  this  phenomenon  of  lessened  liver  dullness  is 
mainly  due  to  an  alteration  in  the  degree  of  distension  of  the 
liver  tissue  rather  than  to  the  other  factors  mentioned,  p.  191. 

Cardiac  asthenia  of  rheumatic  origin  and  small  liver 
dullness,  p,  (195). 

4.  Evidence  as  to  the  emptiness  of  the  auriculo-venous 
reservoir  must  be  looked  for  by  examination  of  the  one  place 
where  direct  clinical  study  of  its  condition  is  possible — namely, 
the  so-called  jugular  bulb,  where  the  external  jugular  vein 
opens  into  the  subclavian,  pp.  133, 137. 

A  lessening  in  the  volume  of  the  jugular  bulb  pulsation 
(as  palpable  behind  the  clavicle)  is  suggestive  of  compensatory 
diminution  in  the  fullness  of  the  reservoir. 

Where  lessened  vigour  of  pulsation  accompanies  the 
lessening  in  volume  it  suggests  that  cardiac  weakness  is  the 
cause  of  the  compensatory  lessening  of  the  blood  volume, 
p.  97. 

Where  cardiac  weakness  is  considerable  the  jugular  bulb 
pulsation  is  no  longer  palpable,  pp.  137  and  138. 

5.  Emptiness  of  the  veins  is  also  a  sign  that  there  is  com- 
pensatory diminution  in  the  volume  of  blood  in  circulation, 
p.  132.  ^ 

In  the  case  of  the  veins  at  the  root  of  the  neck,  important 
evidence  may  be  given  by  their  emptiness  in  the  case  of  cardiac 
weakness,  pp.  57,  61,  95, 187. 

Emptiness  of  the  neck  veins  is  of  considerable  diagnostic 
importance  when  it  occurs  under  circumstances  that  might 
be  expected  to  result  in  their  over-distension. 


584  HUMMAKY 

Emptiness  of  the  neck  veins  in  pneumonia  a  sign  of 
dangerous  myocardial  weakness,  pp.  (97),  (105). 

Emptiness  of  the  venous  system  shown  by  the  occurrence 
of  dyspnoea  on  the  apphcation  of  the  armlet  of  the  sphygmo- 
manometer, p.  140. 

Summary  of  Facts  and  Arguments  in  Connection  with 

THE    AUEICULO-VENOUS    EesERVOIR 

It  is  a  compensation  reservoir  for  the  supply  of  blood  to 
the  right  ventricle,  p.  132. 

Anatomical  Considerations 

The  reservoir  is  constituted  by — 

1.  The  right  auricle. 

2.  The   superior   vena   cava,   innominate   veins,    and   the 

first  part  of  the  subclavian  veins. 

3.  The  vena  azygos  and  its  branches. 

It  is  enclosed  within  certain  valves — namely  : — 

1.  The  Eustachian  valve  guarding  the  inferior  vena  cava. 

2.  The  venous  valves  which  prevent  a  reflux  into  the  distal 
veins.  Chief  ones  are  those  in  the  subclavians  and  those  at 
the  mouth  of  the  internal  and  external  jugular  veins,  and 
those  of  the  azygos  system. 

Physiological  Considerations 

Tonic  activity  of  its  walls. 

1.  The  muscular  walls  of  the  auricle  and  the  veins  are 

possessed  of  tonic  activity  Avhereby  the  blood  in  the 
reservoir  is  maintained  at  a  definite  minimal  pressure, 
pp.  133,  503. 

2.  In  order  to  do  this  the  muscular  walls  must  respond 

by  increased  tonic  activity  to  any  tendency  to  the 
lowering  of  the  blood  pressure.  The  muscular  fibres 
must  therefore  be  sensitive  to  mechanical  stimulation 
by  relaxation  of  their  tension,  p.  507. 

3.  The  muscular  walls,  in  virtue  of   their  tonic  activity, 

also  endeavour  to  counteract  the  tendency  to  dilatation 


THE  AURICULO-VENOUS  RESERVOIR  585 

of  the  reservoir  which  would  result  from  any  excess 
of  blood  pressure  within  it. 
4.  To  accomplish  this  the  muscular  walls  of  the  auricle 
and  the  veins  are  sensitive  to  mechanical  stimulation, 
by  stretching,  and  respond  by  increased  tone  to  any 
force  tending  to  dilate  it,  pp.  37,  504,  506. 

Contractile  activity  of  the  muscular  walls  of  the  reservoir. 
As  regards  the  auricle. 

1.  It  contracts  in  response  to  nodal   stimulation  at  a 

time  wlien  it  is  only  half- full,  just  prior  to  the 
ventricular  systole — the  so-called  auricular  systole. 
The  most  effective  part  of  this  contraction — is  the 
contraction  of  the  auricular  appendix  whereby  (a) 
the  filling  of  the  ventricles  is  completed,  (h)  the 
auriculo-ventricular  valves  are  made  tense  in 
preparation  for  the  ventricular  systole,  and  (c)  in 
all  probabiHty  the  stretching  of  the  ventricular 
walls  by  the  sudden  entry  of  blood  from  the  auricle 
adds  a  meclianical '  stimulus-to-contract '  to  the  nodal 
one.  The  contraction  of  the  appendix  is  the  spark 
that  fires  the  powder  and  determines  the  exact 
time  of  the  occurrence  of  the  ventricular  systole. 
Irregularity  of  rhythm  characterises  a  fibrillating 
auricle,  p.  529. 

2.  The  muscular  wall    of    the    auricle    is    sensitive  to 

mechanical  stimulation  by  stretching  of  its  walls, 
and  a  true  contraction  may  result  if  the  distension 
be  sudden  enough  and  powerful  enough  (such  a 
contraction  may  be  detected  by  the  cardiograph 
in  right  ventricular  tracings  if  the  distending  force 
be  not  so  powerful  or  so  prolonged  as  to  prevent 
the  auricle  from  throwing  blood  into  the  ventricle), 
pp.  504,  515. 

3.  The  auricle  wall  can  also  be  stimulated  mechanically 

to  a  prolonged  contraction  if  the  distending  force 

•     be  maintained.     Thus  in  tricuspid  regurgitation,  in 

the  rare  cases  wdiere  tracings  can  be  taken  from  the 

body  of  the  auricle,  it  is  found  sometimes  that  the 


586  SUMMARY 

auricle  does  not  become  distended  by  the  regurgita- 
ting blood  till  towards  the  end  of  the  ventricular 
systole,  pp.  509,  521. 
4.  It  is  also  probable  that  the  muscular  walls  of  the 
auricle  may  be  stinmlated  to  develop  a  true 
contractile  act  (as  distinct  from  a  mere  increase  of 
tonicity)  by  a  sudden  relief  of  tension  such  as  takes 
place  when  its  contents  are  aspirated  into  the 
ventricle  during  the  expansion  phase  of  the  cardiac 
cycle. 

As  regards  the  venous  portion  of  the  reservoir. 

1.  The  walls  of  the  great  veins  which  constitute  a  portion 

of  the  reservoir  are  stimulated  to  contract  by  a 
distensile  force  of  adequate  suddenness  and  power. 
Such  a  contraction  may  be  observable  in  tracings 
taken  over  the  jugular  bulb,  provided  that  the  force 
is  not  sufficiently  powerful  to  overcome  the  muscular 
power  of  the  veins  nor  sufficiently  prolonged  to 
prevent  the  contraction  from  emptjdng  the  veins. 
(Such  a  contraction  may  be  demonstrable  in  cases 
where  an  extra  systole  causes  forcible  tricuspid 
regurgitation  of  small  volume),  p.  506,  fig.  160, 
p.  513,  point  10. 

2.  These  veins  are  also  stimulated  to  a  true  contractile 

act  by  a  sudden  relief  of  tension  within  them.  Such 
a  contraction  is  observable  in  tracings  taken  over  the 
jugular  bulb  when  a  distended  reservoir  is  suddenly 
emptied  during  the  auricular  expansion  phase  which 
follows  its  systole,  p.  508,  fig.  160,  point  2. 

As  regards  the  relationship  of  the  right  ventricle  during 
its  relaxation  phase  to  the  auriculo-venous  reservoir. 

During  its  '  relaxation  phase  '  the  right  ventricle  contains 
the  blood  aspirated  into  it  during  its  expansion  phase, 
and  this  blood  does  apparently  constitute  a  part  of 
the  contents  of  the  reservoir.  The  walls  of  the  right 
ventricle  are,  during  the  '  relaxation  phase,'-  main- 
tained in  a  state  of  tonic  contractility  and  the  blood 
within  it  is  maintained  thereby  at  the  same  pressure 


THE  AURICULO-VENOUS  RESERVOIR  587 

as  that  in  the  aiiriculo-venoiis  reservoir  proper, 
p.  513. 

Moreover,  there  is  reason  to  beheve  that  during  its 
relaxation  phase  the  walls  of  the  ventricle  are  sensi- 
tive to  mechanical  stimulation  and  a  true  contraction 
can  be  originated  by  sudden  distension  with  blood, 
p.  497. 

During  the  relaxation  phase  it  is  probable  that 
the  tonic  power  of  the  walls  of  the  ventricle  is  less 
than  that  of  the  auricle  and  the  veins,  and  that  by 
this  means  the  blood  which  has  been  aspirated  into 
the  ventricle  is  maintained  within  it. 

Other  physiological  points  in  connection  with  the  auriclo- 
venous  reservoir  in  health  and  disease. 

1.  The  venous  valves  may  be  considered  an  integral  part 
of  the  cardiac  mechanism, 
(a)  Their   presence   admits    of    the   maintenance   of  a 
moderately  high  blood-pressure  within  the  reservoir. 
The  presence  of  this  definite  blood  pressure  within 
the  reservoir  is  evidenced  by  the  fact  that  when 
tracings  are  taken  simultaneously  over  the  reservoir 
l)ehind  the  clavicle  and  over  the  right  ventricle  the 
conduction  of  impulses  through  the  blood  in  the 
reservoir  is  practically  instantaneous,  p.  503. 
(6)  They   admit   of   the   utilisation  of   the  respiratory 
movements  for  the  filling  of  the  right  ventricle,  p.  13. 
Inspiration  tends  to  fill  the  reservoir,  and  expi- 
ration to  empty  it  into  the  ventricle.     As  evidence 
of   this,  the   first  cardiac  beat  that  occurs  during 
expiration    is    (so  far    as    the    right    ventricle    is 
concerned)  more  effective  than  those   during    the 
remainder    of    the  respiratory   cycle  ;    for   cardiac 
sounds  and  murmurs,  and  cardiac  pulsation  due  to 
this  beat,  are  demonstrably  louder  than  the  others, 
p.  13. 

The  effect  of  deep  sighing  respirations  in  aiding 
a  failing  right  ventricle  depends  upon  this  pheno- 
menon, p.  13. 


588  SUMMARY 

(c)  Tliey,  in  conjunction  with  the  tonic  contractihty  of 
the  walls  of  the  veins  and  of  the  auricle,  hinder 
tricuspid  regurgitation  and  thus  can  give  support  to 
the  right  ventricle  when  overtaxed,  p.  37. 

2.  The  tonic  contractility  of  the  auricle  and  veins  retains 

in  the  relaxed  ventricle  the  blood  that  it  aspirated  into 
itself  during  its  expansion  phase. 

3.  The  fact  that  the  superior  vena  cava  is  in  close  anatomical 

contact  with  the  ascending  aorta,  results  in  the  com- 
pression of  the  vein  by  the  sudden  distension  of  the 
first  part  of  the  aorta  which  takes  place  at  the  com- 
mencement of  the  ventricular  systole. 

The  sudden  rise  in  venous  pressure  due  to  this  com- 
pression is  evidenced  in  tracings  taken  over  the  so- 
called  jugular  bulb  by  a  systolic  wave  in  the  venous 
tracing  which  is  synchronous  with  the  sj^stolic  wave 
in  the  ventricular  tracing  due  to  the  return  of  blood 
from  the  distended  first  part  of  the  aorta  (i.e.  with 
the  '  first  aortic'  or  recoil  wave),  pp.  512,  531. 

4.  The  functions  of  the  azygos  vein  in  relation  to  the 

auriculo-venous  reservoir. 

In  consequence  of  the  ineffectiveness  of  the  valves 
in  this  vein  and  the  relationship  of  its  intercostal 
tributaries  with  the  anterior  thoracic  veins,  it  is 
probable  that  it  acts  as  a  safety-valve-like  outlet  to 
the  reservoir. 

Physiology  of  the  auriculo-venous  reservoir  in  relation  to 
the  phases  of  the  cardiac  cycle. 

These  are  fully  summarised  at  p.  528. 

Pathological  changes  in  the  reservoir. 
1.  As  regards  the  right  auricle. 

Dilatation  in  tricuspid  incompetence. 

Dilatation  takes  place  to  the  right  and  backwards, 

and,  owing  to  its  association  with  dilatation  of  the 

ventricle,  a  dilated  auricle  very  rarely  indeed  comes 

into  close  relationship  to  the  anterior  chest  wall,  p.  41. 

Its  dilatation  may  lead  to  incompetence  of  the 


THE  AURICULO-VENOUS  RESERVOIR  589 

Eustachian  valve  and  engorgement  of    the  hepatic 
vein,  p.  39. 

Dilatation  sometimes  very  excessive,  p.  (210). 
The    membranous  lower  portion  is   sometimes 
greatly  dilated,  p.  (210). 
2.  As  regards  the  great  veins. 

Their  dilatation  in  tricuspid  regurgitation  sometimes 
give  rise  to  distinct  pulsation  in  the  episternal  and 
supra-clavicular  fossae  ;  also  in  the  veins  of  the  neck 
through  incompetence  of  the  valves. 
The  dilatation  of  the  superior  cava  is  less  at  the  point 
where  it  passes  through  the  pericardium  than 
elsewhere,  and  thus  a  constriction  is  caused  in  the 
vein,  at  which  a  murmur  can  arise.  This  may  be 
called  the  '  superior  vena  cava  murmur,'  pp.  44,  218. 

Clinical  Phenomena  associated  with  Pathological 

CONDITIONS    of 

I.  The  right  auricle. 

(1)  When  dilated  it  is  very  rarely  indeed  recognisable 

by  palpation  or  percussion  anteriorly,  owing  to  the 
direction  in  which  it  usually  dilates,  p.  41. 

When  considerably  dilated  there  may  be  increased 
loudness  of  the  heart  sounds  over  the  ninth  and 
tenth  interspaces  to  the  right  of  the  spine  or  in  the 
right  axilla,  p.  42. 

(2)  Dilatation  of  the  lower  part  of  the  auricle  may  lead 

to  incompetence  of  the  Eustachian  valve  and  thus 
allow  of  tricuspid  regurgitation  into  the  liver  and 
the  physical  signs  to  which  this  gives  rise,  p.  39. 

II.  Of  the  superior  vena  cava. 

The  only  definite  sign  associated  with  this  condition 
is  the  superior  vena  cava  murmur  which  may  give 
valuable  evidence  as  to  the  presence  of  tricuspid 
regurgitation,  pp.  44,  218. 

III.  Of  the  great  veins. 

(«)  The  closure  of  the  venous  valves  when  due  to  tricuspid 
regurgitation  may  very  occasionally  give  rise  to  a 
definite  sound,  p.  220. 


590  SUMMARY 

{h)  The  incompetence  of  the  valves  not  infrequently 
gives  rise  to  a  systohc  murmur,  p.  219,  (291). 

(c)  The  over-distension  of  the  veins  may  give  rise  to 
pulsation  in  the  supra-clavicular  fossae  or  the  epi- 
sternal  notch,  p.  134. 

{(T)  Incompetence  of  the  venous  valves  will  give  rise  to 
distension  of,  and  systolic  pulsation  in,  the  veins 
of  the  neck,  pp.  39,  137. 

(e)  When  the  azygos  vein  is  over-distended  as  a  result  of 
tricuspid  incompetence  this  may  show  clinically 
by  distension  of  some  of  the  intercostal  veins,  also 
any  sudden  increase  of  intrathoracic  pressure — 
such  as  that  due  to  coughing — may  cause  a  recog- 
nisable impulse  in  one  or  more  of  them. 

Clinical  phenomena  showing  the  condition  of  the  auriculo- 
venous  reservoir. 

Direct  study  of  the  condition  of  the  reservoir.  When 
normal  there  is  only  one  point  at  which  the  condition 
of  the  reservoir  can  be  directly  studied  clinically — 
namely,  at  the  point  where  the  external  jugular  vein 
opens  into  the  subclavian.  The  limiting  valve  is  a 
short  distance  up  the  vein,  and  the  portion  on  the 
proximal  side  of  the  valve  is  within  reach  of  the 
finger — if  pressed  well  down  behind  the  clavicle. 
This  portion  of  the  vein  is  called  by  Sir  James 
Mackenzie  the  jugular  bulb,  p.  133. 

Pulsation  in  jugular  bulb  a  true  venous  pulse,  p.  134. 

Its  importance,  pp.  39,  132,  137. 

Its  fullness  or  emptiness  shows  the  fullness  of  the  amiculo- 
venous  reservoir,  p.  134. 

Its  tension  shows  the  tension  of  the  blood  in  the  reservoir  ; 
a  low  tension  being  suggestive  of  heart  weakness. 

The  volume  of  the  pulsation  in  excess  of  normal  shows 
the  amount  of  tricuspid  leakage. 

The  force  of  the  pulsation  is  a  most  important  guide  to  the 
strength  of  the  right  ventricle,  pp.  (88),  133. 

Jugular  l»ulb  pulsation  a  surer  guide  to  the  strength  of  the 
right  ventricle  in  later  life  than  the  arterial  pulse  is 
to  that  of  the  left  ventricle,  p.  134. 


THE  AURICULO-VENOUS  RESERVOIR  591 

When  abnormally  full  the  distended  veins  become  palpable 
and  dilatation  and  pulsation  of  the  neck  veins  will 
occm-. 

The  condition  of  the  auriculo-venous  reservoir  can  also  be 
studied  indirectl}''. 
The  indirect  stud}'  of  the  state  of  the  reservoir  is  possible, 
because  when  overfull  its  distension  is  as  a  rule 
associated  with  overfuUness  of  the  right  heart  and 
of  the  lungs,  and  when  undul}^  empty  its  underfilling 
is  associated  with  relative  emptiness  of  the  heart 
and  of  the  lungs. 

This  increase  or  decrease  in  the  volume  of  the 
intrathoracic  contents  can  be  detected  chnically  by 
observing  the  state  of  the  two  non-rigid  portions 
of  its  walls — namely,  the  floor  as  constituted  by  the 
diaphragm,  and  the  upper  boundary  which  consists 
of  the  soft  tissues  in  the  supra-clavicular  fossae, 
p.  163. 

When  the  tissues  of  the  diaphragm  are  sufficiently 
yielding  and  elastic  (as  in  the  earher  decades  of  life) 
an  alteration  in  its  level  will  provide  adequate 
compensation  for  variations  in  the  volume  of  the 
thoracic  contents,  p.  94. 

"\Mien,  as  in  later  life  its  tissues  are  more  rigid, 
evidence  as  to  the  fullness  or  emptiness  of  the 
reservoir  is  also  given  by  fullness  or  hollowdng 
above  the  clavicles,  p.  94. 
Fullness  of  the  reservoir,  such  as  results  from  cardiac 
failure,  accompanied  by  tricuspid  regurgitation,  will 
show  chnically,  when  the  tissues  are  soft  and 
resilient,  l)y  lowness  of  both  sides  of  the  diaphragm — 
namel}',  lowness  of  the  upper  level  of  the  liver  dullness 
on  the  right  and  of  the  gastric  resonance  on  the  left, 
with  downward  displacement  of  the  heart,  pp.  (318), 
363,  (364),  (366). 

And  to  a  less  extent  by  filling-up  of  the  supra- 
clavicular hollows. 
When  tissues  are  more  rigid,  there  will   be   less  altera- 


592  SUMMARY 

tion  in  level  of  diaphragm  and  more  filling  of 
supra-clavicular  hollows,  pp.  94,  134. 

Emptiness  of  the  reservoir  (in  common  with  the  vessels 
of  the  lungs)  will  occur  whenever  there  is  compensa- 
tory lessening  of  the  amount  of  blood  m  circulation 
(see  '  Blood  Volume,  Compensatory  Lessening  of ' 
p.  577),  p.  57. 

This  will  be  shown  clinically  by  the  signs  of  diminution 
in  the  size  of  the  intrathoracic  cavity,  which  are 
summarised,  at  p.  579. 

Summary  and  Index  of  Arguments  and  Facts  relating  to 
Compensatory  Phenomena  in  connection  with  the 
Heart  and  Blood-vessels 

In  Connection  with  the  Great  Veins 

The  amicle  and  great  veins  constitute  a  compensation 
reservoir  for  the  right  ventricle,  p.  2. 

The  tonic  and  contractile  activity  of  the  walls  of  the  auricle 
and  veins  by  tending  to  check  tricuspid  regm'gitation  help  to 
compensate  for  incompetence  of  the  tricuspid  valve,  pp.  13, 
37,  133,  509,  521. 

The  inefficiency  of  the  valves  in  the  azygos  vein  and  its 
branches  enables  it,  in  all  probabihty,  to  act  as  a  safety- 
valve-like  outlet  to  the  auriculo-venous  reservou-,  whenever 
there  is  a  sudden  tendency  to  its  over -distension  with  blood  or 
to  the  blood  pressure  in  it  being  unduly  raised — as  in  the  act 
of  coughing. 

In  Connection  with  the  Blood-vessels 

In  extreme  myocardial  weakness  there  is  compensatory 
contraction  of  the  peripheral  arterioles  so  as  to  maintain  the 
low  blood  pressure  at  its  maximal  height  throughout  the 
diastole,  59. 

Weak  pulse  of  high  tension  in  enteric  fever,  p.  59. 

In  extreme  heart  weakness  there  is  compensatory  contrac- 
tion of  the  peripheral  vessels  so  as  to  give  a  maximal  supply 
of  blood  to  important  organs,  p.  109. 


COMPENSATORY  PHENOMENA  593 

Pallor  of  the  face  in  fainting,  and  in  some  cases  of 
defective  compensation  in  valvular  disease,  p.  450, 

In  myocardial  weakness  there  is  compensatory  diminution 
in  the  amount  of  blood  in  the  peripheral  circulation.  Case 
demonstrating  this,  p.  (140). 

When  there  is  great  hmitation  in  the  amount  of  blood 
available  for  the  left  ventricle  (e.g.  where  there  is  fatty  degenera- 
tion of  the  right  ventricle  and  the  left  one  is  strong)  there  is 
compensatory  increase  in  the  force  and  the  suddenness  of  the 
pulse  wave,  p.  (156). 

Strong  collapsing  pulse,  showing  fatty  degeneration  of  the 
right  ventricle  with  a  strong  left  ventricle,  p.  (155). 

Compensatory  rise  in  the  blood  pressm-e  where,  from 
disease  of  the  coronary  arteries  or  other  cause,  a  normal  blood 
pressure  does  not  suffice  adequately  to  nourish  the  heart 
muscle,  p.  144. 

Characters  of  compensatory  rise  in  the  blood  pressure  as 
shown  by  the  sphygmo-oscillometer,  p.  144. 


Compensatory  Diminution  in  the  Amount  of  Blood  in 
Active  Circulation  in  Heart  Weakness.  (See  special 
summaiy,  p.  577.) 

Compensatory  Phenomena  Connected  with  the  Heart 

In  overstrain  of  a  ventricle  the  stretcliiug  of  the  am-iculo- 
ventricular  orifice  allows  regurgitation  to  take  place  and  thus 
checks  the  tendency  to  fm'ther  dilatation  of  the  ventricle, 
p.  32. 

In  myocardial  weakness  the  inefficiency  of  the  ventricular 
contraction  results  in  a  compensatory  diminution  in  the 
amount  of  blood  in  active  circulation,  pp.  50,  180,  185. 

When  (as  in  adolescence)  the  tissues  of  the  heart  are 
relatively  elastic,  muscular  weakness  is  accompanied  by  a 
compensatory  diminution  in  the  filHng  of  the  heart,  p.  53. 

This  causes  a  diminution  in  the  size  of  the  heart,  as  observed 
clinically.  A  condition  which  may  be  called  '  heart 
failure  with  small  heart,'  p.  54. 


594  SUMMARY 

Compensatory  Phenomena  in   connection  with  the 
Eight  Ventricle 

Compensatory  overaction  of  the  right  heart  often  constitutes 
the  iirst  cKnical  sign  that  the  left  ventricle  is  being  overtaxed, 
pp.  2,  46. 

In  valvular  disease  of  the  left  side  the  amount  of  com- 
pensatory overaction  of  the  right  ventricle  is  a  measure 
of  the  extent  to  which  the  left  ventricle  is  faihng  to  com- 
pensate for  the  valvular  defect,  pp.  47,  422. 

Compensatory  Phenomena  connected  with  the  Left 
Ventricle 

Compensation  for  valvular  regm-gitation.     Its  nature. 

Dilatation  and  hypertrophy  commensurable  mth  the 
amount  of  valvular  leakage  are  necessary,  pp.  389,  412. 

Importance  of  cardiac  distensibihty  in  admitting  of 
adequate  compensatory  dilatation,  pp.  11,  150. 

Softening  effect  of  rheumatism  upon  the  heart  is  of  impor- 
tance in  aiding  the  development  of  compensation,  pp.  ii,  343. 

Eigidity  of  the  heart  wall  a  cause  of  faulty  compensation, 
p.  452. 

Adherent  pericardium  interfering  with  compensation,  pp. 
397,  (433),  (455). 

Eelative  rigidity  of  the  heart  in  later  hfe  interfering  with 
compensation  for  valvular  disease,  p.  (456). 

Pallor  a  sign  of  faulty  compensation,  pp.  450,  &c. 

Cardiolysis  a  remedy  for  the  imperfect  compensation  that 
may  result  from  adherent  pericardium,  p.  457. 

Compensation  in  Aortic  Eegurgitation,  p.  347 

Compensatory  diminution  in  the  amount  of  aspnation  is 
shown  by  weakness  of  the  hist  sound  and  by  cardiographic 
evidence,  p.  409. 

Compensation  in  Mitral  Eegurgitation 

When  perfect  it  depends  on  the  left  ventricle  alone  not  on 
the  right,  p.  412. 

Extra  work  is  only  thrown  on  the  right  side  of  the  heart 
when  compensation,  from  any  cause,  is  imperfect,  pp.  389,  422. 


COMPENSATOEY  PHENOMENA  595 

The  ventricle  develops  suJBdcient  hypertrophy  and  dilatation 
to  compensate  for  the  valvular  leakage,  p.  389. 

The  hypertrophy  and  dilatation  necessary  for  the  proper 
emptying  of  the  ventricle  is  also  adequate  for  its  proper  filling, 
pp.  389,  412,  417. 

No  extra  work  is  thrown  on  the  right  ventricle  when  com- 
pensation is  perfect,  pp.  417,  (4'22). 

Pulmonary  second  sound  not  increased  in  loudness,  pp.  389, 
(422),  (424).   _ 

No  dilatation  of  the  left  auricle,  pp.  402,  417. 

Development  of  compensatory  dilatation  of  the  ventricle 
by  means  of  its  own  aspiratory  force,  p.  397. 

Cases  demonstrating  the  increased  aspu-atory  force  which 
the  ventricle  ccm  develop  in  mitral  regm-gitation, 
p.  (433). 

Expansion  phase  well  marked  in  the  cardiogram,  pp.  385, 
403,  440,  Plate  XII. 

Evidences  of  overaction  of  the  right  ventricle,  which  are 
characteristic  of  faihng  compensation,  disappear  when  it 
becomes  perfect,  p.  (423). 

Cases  showing  great  dilatation  of  the  left  auricle  where 
compensation  was  imperfect,  pp.  433,  455. 

Compensation  in  Mitral  Stenosis 

The  left  ventricle  alters  its  mode  of  contraction  so  as  *to 
increase  its  aspkatory  power  both  muscular  and  mechanical, 
pp.  396,  405,  418,  (423). 

Its  contractile  force  is  concentrated  at  the  end  of  systole, 

pp.  390,  419. 
The  characteristic  sharp  ending  of  the  fii'st  sound  in  stenosis 

is  thereby  explained,  pp.  390,  418. 
Its  contractile  force  is  increased  in  order  to  increase  at  the 
same  time  its  expansile  force,  pp.  405,  418. 

The  first  sound  is  therefore  abnormally  loud,  pp.  390,  405, 
418,  (423),  (425). 

Failure  of  compensation  or  temporary  embarrassment 
increases  the  loudness  of  the  first  sound  very  greatly 
and  it  lessens  as  compensation  improves,  pp.  419, 
(423),  (425). 

2q  2 


596  SUMMARY 

This  increased  force  explains  the  hypertrophy  of  the  left 
ventricle  which  is  sometimes  recognisable  in  mitral 
stenosis,  pp.  391,  418. 
Evidence  of  increased  aspiration  m  mitral  stenosis  is  given 
of  the  cardiograph,  p.  406. 

'  Suction  recoil '  wave  in  the  cardiogram,  pp.  407,  428,  (432). 

The  increased  aspu-atory  force  thus  developed  compensates 

for    the    narrowing  of    the    mitral    orifice,  and    there    is  no 

hindrance  to  the  circulation  through  the  lungs,  pp.  391,  419. 

The  left  auricle  is  often  found  to  be  normal  in  cases  dying 

without  loss  of  compensation,  pp.  391,  419. 
The  right  ventricle  does  not  have  extra  work  thrown  upon 

it  in  compensated  mitral  stenosis,  pp.  406,  420. 
The  true  loudness  of  the  pulmonary  second  sound  is  not 
greater  than  normal  in  compensated  mitral  stenosis, 
pp.  391,420,(425),  (426). 
When    compensation   is    imperfect    the    second    sound    is 
accentuated,  but  lessens  in  loudness  as  compensation  improves, 
pp.  420,  (422). 

The  well-known  '  accentuated  second  sound  '  of  mitral 
stenosis  is  a  '  spurious  accentuation  '  due  to  the  right  ventricle 
adopting  the  same  type  of  forcible  beat  which  the  left 
ventricle  has  to  adopt,  pp.  392,  423,  and  424  footnotes. 

Pulmonary  second  sound  much  louder  in  anaemia  or  uncom- 
pensated valvular  disease  than  in  compensated  mitral  stenosis, 
pp.  392,  415,  (421). 


PLATE   IX 
Tracing    No.   1 


^ept.  ie^^i3o&.    0 


Rig-ht     car  otic 


Tracing    No.  2 


icing- S- 
\uiias 


S'       K' r 


Tracing    No.  3 


H^ 


tion 

JJxpiratioiz 


EXPLANATION    OF    THE    TRACINGS 

Each  division  ol  the  timu  record  represents  one-fifth 
of   a  second. 

Tracing  No.  1. — Showing  a  tracing  taken  just  internal 
to  the  apes  beat  compared  with  one  taken  over  the  carotid 
artery.  These  tracings  were  taken  shortly  after  admission 
to  the  hospital.  Note  the  frequence  of  the  extra  systoles, 
and  the  fact  that  no  wave  is  caused  in  the  carotid  artery 
by  the  extra  systole,  and  that  the  fullness  of  the  carotid 
beat  which  follows  an  extra  systole  is  often  less  than  normal. 


Tracing  No.  2. — A  tracing  taken  at  the  apex  on  which 
was  recorded  the  time  of  occurrence  of  the  first  and  second 
heart  sounds  by  means  of  an  electric  signal.  The  corre- 
sponding points  on  the  two  tracings  are  shown  by  the 
lines  that  have  been  ruled  between  them.  The  timing  is 
not  always  accurate  owing  to  the  irregularity  of  the  heart. 
It  is,  however,  sufficiently  accurate  to  show  that  the  time 
of  occurrence  of  the  second  sound  corresponds  with  the 
last  wave  of  the  apex  cardiogram  just  before  tho  final  fall  of 
the  tracing  to  normal. 


Tbaoino  No.  3. — The  upper  tracing  is  an  apex  cardio- 
gram, and  the  lower  one  from  the  jugular  bulb.  Note  that 
the  extra  systole  only  occurs  at  the  end  of  inspiration. 
Corresponding  points  on  the  two  tracings  are  connected  by 
dotted  lines. 


PLATE  IX 
rRACINO    No.    1 


Apex 


Just  intern&J  totspex  Jbea.t.       Sept  le^^  190Q .     On  7Y.  Bel 7(3. donna     ni  iv. 


N?i 


Tracing   No.  3 


m^ 


Inspiration^  \r    Inspiration 

Expiration.  ^lxpir3,tioii 


Tracing   No.  4 


Tracing  No.  4. — Tho  upper  tracing  is  from  the  apex  ; 
the  lower  from  the  jugular  bulb.  The  early  part  shows 
the  effect  of  aconite  in  lessening  the  frequency  of  the  extra 
systoles.  In  the  latter  part  the  rhythm  changes  and  there 
is  an  extra  systole  after  each  beat. 


N^i!. 


US  traciJcing  shown  in  Plate  Xa  opposite, 
be  veriqjj  t^ig  essay. 


PLATE  X 
Tracisg  No. 


with  fill  the  others  here  g 


n  Plate  X 

y  perfect,  but  s 


^"^C'T.C-^VJ 


Xhifar  enough  for  satisfactory  reproduction, 
in  Plate  X. 


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PLATE  XI 

No.  0 


Tracixq  No.  7.— This  shuws  a  tracing  lukon  a  littlo 
intonial  to  tlio  apDx  beat  coinparod  with  ono  takonovor  lliQ 
jugular  bulb  while  tho  hoart  woa  under  tho  inlluenco  of  di^i- 
tiilis.     Another  portion  of  tliLa  tracing  U  showD  in  fig.  15U, 


Tracixo  No.  8. — This  shows  a  tracing  taken  a  little  in- 
ternal to  the  apex  beat  ooinparod  with  one  taken  over  tbo 
jugular    bulb,    while    tho    heart    wae   strongly   under  tho 
influence  of  digitalis.     Linos  are  roled  between  the 
sponding    poinbs    on    tho    two    tracings.     This    tracing 
uxplninod  at  p,  i>l<J. 


r 


PLATE  XII 
Auricular  and  V^entricular  Tr 


2-1  l^^l 

•^  t!       O  0,   1J  >f 


Second  Sounds 


I' LATE  XII 

B  AND  VeSTRICCLAR  Tra( 


EXPLANATION     OF    THE    TRACINGS 


raoiogB  are  Erom  the 
ispid  rogurgitatioD.  which  ie  referred  to  . 
and  404.  and  ol  whioh  cardiogramB  are  given 


Tbacimo  No.  9.— Showa  a  cardiogram  taken  just 
iotornal  to  the  apex  and  a  tracing  taken  eimultaaeously 
over  tbo  right  auricle.  These  tracings  are  explained  at  p.  5:^1. 


Teaciso    No.     10.— Cardiogi 

3  the  Bpox  with  the  time  of  occurrence  of  llio 
heart  sounds  recorded  on  it.  Note  the  marked  axpaiiKi'ni 
rise  following  tho  main  systolic  rise.  The  irregularity  ol 
the  heart  has  made  tho  timing  of  tbo  eounda  rnlluT 
difficult,  and  tho  first  Bound  is  very  rarely  accurate.  It 
ought  to  occur  just  after  the  commencement  of  the  systolic 
i  4,  7,  11,  12.  and  13  shown.  The  aocnnd 
sound  was  natorally  more  ooay  to  time  and  shows  less 
I  tho  first ;  the  most  accurate  position  for  it 
1  that  shown  in  beats  2,  3,  4,  7,  fl,  II,  12,  and  Vi. 


K 


SUBJECT   INDEX 


Figures  in  black  tj-pe  refer  to  important  references. 
Figures  in  small  type,  refer  to  ordinary  references. 
Figures  in  parentheses  (8)  refer  to  references  to  clinical  cases. 
Figures  above  532  refer  to  the  Summary. 

'  Absolute  '  overstrain,  310,  342 

Absolute  percussion  dullness,  definition  of  term,  &c.,  21 

„  „         of  heart,  upward  increase  of,  in  ana;mia,  &c.,  25,  228 

„  ,,         disappearance  of,  in  myocardial  weakness,  56,  (119) 

„  „         of  liver :    its  value  as  a  guide  to  the  amount  of  blood 

in  circulation,  185 
„  ,,  ,,         its  decrease  due  to  altered  conductivity  of  the 

liver  tissue  when  relaxed,  191 
,,  „  „  its  diminution  a  valuable  sign  of  heart  weak- 

ness, 195 
Accentuation  of  the  first  sound  of  the  heart  in  mitral  stenosis  a  compensatory 
phenomenon,  390,  425 
„  of  the  right  ventricle  first  sound  an  evidence  of   failure  of  the 

left  ventricle,  47 
,,  of  the  aortic  second  sound  in  disease  of  the  mitral  valve  due  to 

increased  aspiration,  418,  423 
„  of  the  pulmonary  second  sound  in  ana?mia,  244,  337,  415,  421 

„  „  „  „  „      in  failing  compensation  for  val- 

vular disease,  422 
„  „  „  .,  „      in  compensated  mitral  stenosis 

is  reallv  a  false  accentuation, 
392,  423,  424 
Adherent  pericardium  :   physical  signs  of,  454 

„  ,,  a  cause  of  defective  compensation  in  mitral  regur- 

gitation, (433),  (454),  (455) 
Adhesions  Limiting  the  distensibility  of  the  right  ventricle  a  cause  of  sudden 

death,  especially  under  anaesthesia,  62 
Adolescence,  softness  of  the  fibrous  tissues  in,  8,  10,  535 

„  ,,  „  „  in  relation  to  cardiac  enlargement, 

8,  10 
„  „  „  „  in   relation   to   diminution    in   the 

size  of  the  heart,  50,  54,  537,  567 
„  ,,  „  ,,  in  relation    to    rise  of  diaphragm 

in   compensatory   diminution   of 
the  blood  volume,  72,  94 
„  early  diagnosis  of  cardiac  failure  in,  28 

Adolescent  type  of  cardiac  dilatation,  12,  211,  330,  543 
„  „      pathological  aspects,  247,  546 

„  ,,     clinical  aspects,  547 

„  „     in  aiijemia,  228 

„  „     in  cardiac  overstrain,  309 

Adult  type  of  dilatation  of  the  right  ventricle,  10,  31,  330,  341,  557 


598  SUBJECT   INDEX 

Anemia  and  Heart  Failure. 

Various  relationships  of  heart  failure  to  anaemia,  227,  448 
Anaemia  and  pallor  compared,  450 

Primary  anrcmia  of  adolescence  distinguishable  from  secondary  anaemia  by 
its  type  of  cardiac  dilatation,  243 

ANiEMLV  OF  Adolescexce,  heart  failure  in,  227 

Characteristic  dilatation  iipwards  and  to  the  left,  228 

„  „  due  to  dilatation  of  the  right  ventricle,  232 

Diversity  in  shape  of  the  dilated  heart,  289 
Dilatation  towards  tlie  right  infrequent,  238,  354 
Factors  determining  the  type  and  the  amount  of  the  dilatation,  241,  289 

Overstrain  of  right  ventricle,  243 

Age,  239,  349 

Cardiac  malnutrition,  242 

Left  ventricular  failure  not  a  factor,  240 
Left  ventricular  failure  as  a  rule  infrequent  in  anaemia,  240 

„  „  ,,       sometimes  extreme,  281 

Tricuspid  murmur  infrequent  in  anaemia,  239 
Pulmonary  artor}^  murmur  in,  26,  211,  254,  334 
^lid-diastolic  murmur  and  third  sound  arising  in  right  ventricle,  282,  341 

Aneurysm  of  the  transverse  arch  of  the  aorta : 

Its  diagnosis  from  upward  dilatation  of  the  right  ventricle,  (213) 
A  cause  of  displacement  of  the  heart,  345 
Auemysm,  intra-pericardial  and  displacement  of  the  heart,  (345) 
Aneurysmal  dilatation  of  tlie  pulmonary  artery,  the  cause  of  the  pulmonary 

systolic  murmur,  26,  253 
Angina  pectoris  rare  in  adolescence  and  carlj'  adult  life,  82 

Increasingly  frequent   as   age  advances,   owing  to   increasing   amount  of 

mechanical  aspiration,  36,  82,  126,  567 
Angina  pectoris  of  vasomotor  origin  due  to  colitis,  (127),  (130) 
Aorta,  its  first  part  constitutes  an  expansion  chamber  for  the  left  ventricle : 
Rigidity  of  its  first  part,  a  hindrance  to  the  circulation,  74 

A  cause  of  difficulties  in  diagnosis,  74,  (109) 
Compression  of  the  superior  vena  cava  by  the  systolic  distension  of  its  first 
part,  the  cause  of  the  ventricular  wave  in  the  venous  pulse,  512,  531,  588 
Aortic  '  recoil  waves  '  in  the  ventricular  cardiogram,  501,  512 
Aortic  regurgitation,  principles  of  compensation  in,  347 

Accompanied    by    compensatory   lessening   in   the    amount    of   ventricular 

aspiration,  409 
Accompanied  by  downward  displacement  of  the  heart,  347 
Pallor  a  sign  of  defective  compensation  in,  451 
Lessened  dilatation   and  hypertrophy   a  sign  of  the  onset  of   myocardial 

weakness  in,  (112) 
Presystolic  murmur  of,  iisually  a  mid-diastolic  murmur,  394 
Aortic  regurgitant  murmur,  an  '  expansion  murmur,'  399 

,,  ,,  mid-diastolic  addition  to,  394 

Aortic  second  sound  accentuated  in  mitral  stenosis,  418,  423 
Aortic  systolic  murmur : 

Its  conduction  to  the  back,  444 

Differential  diagnosis  from  an  '  arterial  compression  '  murmur,  226 
From  a  pulmonary  artery  murmur,  215 
From  a  superior  vena  cava  murmur,  218 

Apex  of  the  Heart. 

Displacement  upwards  of  the  apex  of  the  heai't  in  the  adolescent  tvpe  of 
dilatation  of  the  right  ventricle,  19,  234,  348,  (360).  &e. 
Statistics  showing  its  frequency  in  the  heart  failure  of  anaemia,  349 


SUBJECT   INDEX  599 

Apex  op  the  Heart. — Upward  displacement  of  {continued). 

Statistics  showingits  relationship  to  the  amount  of  upward  dilatation,  352 
Showing  that  with  any  given  amount  of  dilatation  the  frequency  of 

elevation  increases  with  age,  350 
Showing  that  its  frequency  is  greater  in  patients  twenty  to  twenty-five 

years  of  age  than  in  younger  patients,  350 
Showing  that  its  frequency  increases  proportionally  to  the  amount  of 

broadening  of  the  right  ventricle  towards  the  left,  352 
Showing  the  absence  of  any  dilatation  to  the  right,  when  the  apex  is 

high,  35-t 

Showing  the  absence  of  a  tricuspid  murmur  when  the  apex  is  high,  355 

Showing  the  absence  of  any  signs  of  left  ventricular  failure  when  the 

apex  is  high,  356 

The  size  of  the  left  ventricle  in  relation  to  the  elevation  of  the  apex,  357 

Diminution  in  the  size  of  the  left  ventricle  a  probable  factor  in  its  causation, 

354 
Stretching  of  the  anterior  wall  of  the  right  ventricle,  as  a  whole,  a  factor 

in  its  causation,  357 
Summary  of  the  agencies  at  work  in  its  causation,  359 
Fixation  points  of  the  heart  in  relation  to  the  upward  displacement  of 

the  apex,  358 
Increase  of  the  right  ventricle  towards  the  left   is   the   actual   cause  of 

the  elevation  of  the  apex,  359 
The  apex  may  sometimes  be  elevated  by  downward  enlargement  of  the 

right  ventricle,  348 
Upward  displacement  in  patient  aged  sixty- two,  (83) 
Displaced  downwards  in  aortic  regurgitation,  346 

In  chronic  venous  congestion  of  the  lungs,  363,  (364) 
Variation  in  its  level  with  change  of  position,  235,  (311),  (312) 

Apex  beat  weak  or  absent  in  myocardial  weakness,  56,  (68),  &c. 
'  Arterial  compression  murmur,'  arising  in  subclavian  artery  in  anajmia,  226, 
281 
Its  diagnosis  from  an  aortic  systolic  murmur,  226 

„  ,,         from  a  venous  valve  murmur,  (291) 

Its  disappearance  on  mo-s-ing  the  shoidder,  226 
Its  artificial  production  by  the  pressure  of  the  stethoscope,  226 
Arterial  pulse : 

Weak  pulse  of  high  tension  diagnostic  of  myocardial  weakness,  e.g.  in  enteric 

fever,  frc,  59 
Normal  or  strong  pulse  in  adult  and  later  life  an  uncertain  guide  to  the  state 

of  the  heart  and  circulation,  35,  143 
Collapsing   high   pressure   pulse  in  fatty   right   ventricle   with  strong  left 
ventricle,  (155) 
Arterial  resistance : 

Its  amount  difficult  to  estimate  in  later  life,  74,  142 
Its  bearing  upon  a  failing  heart  difficult  to  estimate  in  later  life,  142 
Increased  arterial  resistance  sometimes  a  compensatory  phenomenon,  144 
Arterioles,  peripheral,  compensatorUy  contracted  in  great  heart  weakness,  59 
Aspiration  by  the  ventricles  of  the  heart  due  to  transverse  contraction  of 
muscular  fibres  of  its  wall,  384,  400,  412 
In  adolescence  due  to  muscular  expansion  onl_v,  52 
In  adult  and  later  life  mechanical  elastic  recoil  takes  an  increasing  share 

in  the  filling  of  the  ventricles,  53,  78,  79 
Lessened  expansion  in  muscular  weakness  causes  lessened  filling  of  the  heart,  54 
And  compensatory  diminution  in  the  volume  of  the  blood  in  circulation,  55 
Its  compensatory  increase  in  mitral  stenosis,  390,  412 
„  „  „  ,.      regurgitation,  389,  412 

„  „  lessening  in  aortic  reguraitation,  409 


600  SUBJECT   INDEX 

Aspiration  by  auricles  after  their  systole,  508,  512  (point  2),  530 
Asystole — risk  of  death  from — does  not  occur  in  adolescence  because  of  com- 
pensatory underfilling  of  the  ventricles,  53,  82 
Increasing  risk  of  death  from  it  as  age  advances,  owing  to  increasing  amount 
of  mechanical  aspiration,  53,  82,  567 

Auricles. 

Their  muscular  walls  are  sensitive  to  mechanical  stimulation  by  changes  in 

blood  pressure,  504,  507 
By   their  tonic  acti\aty  they  endeavour  to  maintain  a  constant   blood 

pressure  within  the  auricle,  503 
A  definite  contraction  may  result  from — 

1.  Nodal  stimulation,  as  in  the  case  of  the  auricular  systole,  529,  5S5 

2.  From  a  sudden  increase  of  pressure,  as  in  tricuspid  regurgitation,  504 

3.  Probably  also  from  a  sudden  lessening  of  pressure,  as  during  ventri- 

cular aspiration,  528,  586 

4.  A  prolonged  contraction  appears  to  result  from  free  tricuspid  regur- 

gitation, 509,  521 
Their  functions,  387,  528 

1.  To  act  as  a  reservoir  of  supply  to  the  ventricle,  387 

2.  By  their  contraction  ('  systole  ')  to  close  and  stretch  the  auriculo-ventri- 

cular  valves  prior  to  the  ventricular  sj^stole,  388 

3.  To  precipitate  the  ventricular  systole  by  the  mechanical  stimulus  which 

results  from  the  sudden  stretching  of  the  ventricular  walls  by  the  in- 
rush of  blood  from  the  auricle  during  the  auricular  systole,  530,  585 

4.  By  their  tonic  and  contractile  acti\'ity  to  help  to  check  regurgitation 

through  the  auriculo-ventricular  valves,  37,  133,  509,  521 

5.  By  their  tonic  activity  to  maintain  in  the  ventricle  during  the  relaxation 

phase  the  blood  which  was  aspirated  into  it  during  the  expansion 
phase,  528,  587 
Left  auricle : 

Not  very  accessible  to  clinical  examination,  47 

AVhen  dilated  causes  increased  conduction  of  heart  sounds  to  left  inter- 
scapular region,  47,  444 
When  much  dilated  gives  a  dull  percussion  area  in  left  interscapular  region, 

47 
Great  dilatation  in  mitral  disease  with  failing  compensation,  435,  455 
Little  or  no  dilatation  in  mitral  disease  when  compensation  is  good,  402 
Its  appendix  does  not  approach  anterior  chest  wall,  231 
Its  proximity  to  the  vertebrae  admits  of  the  conduction  of  a  mitral  regurgitant 

murmur  down  the  spine,  443 
Right  auricle : 

When  dilated  it  does  not  iisually  approach  the  anterior  chest  wall,  41 

Pulsation  due  to  its  dilatation  very  rarely  observable,  41 

When  dilated  it  may  cause  increased  conduction  of  the  cardiac  sounds  in 

the  lower  dorsal  region  to  the  right  of  the  spine,  42 
Case  showing  extreme  dilatation,  (210),  (339) 
Auricular  appendix,  its  functions,  388,  530,  585 
Auriculo-venous  reservoir,  584 
Auriculo-ventricular   valves,    possibility   of  their  closure   at  the    end    of   the 

expansion  phase,  388 
Austin  Flint  murmur,  394 


Binaural  stethoscope,  theory  of  sound  conduction  by  it,  282 

Light  application  necessary  to  hear  a  third  soimd  of  functional  origin  in 
right  or  left  ventricle,  282 


SUBJECT   INDEX  601 

Blood  Pressure: 

If  high,  there  is  a  varied  relationship  to  cardiac  failure. 

(a)  Due  to  toxic  arterial  resistance  and  throwing  extra  work  on  the  heart. 
High  blood  pressure  from  the  absorption  of  toxins  in  pneumonia,  (103) 
(h)  Compensatory  in  character  and  necessary  for  the  adequate  nutritition 

of  the  heart,  144 
(c)   Compensatory  in  character,  but  insufficient    (owing  to    myocardial 
weakness)  for  the  adequate  nutrition  of  the  heart — compensatory 
distinguishable  from  non-compensatory  by   means  of  the  sph3^gmo- 
oscillometer,  144 
Pathological  variations  in,  a  source  of  diagnostic  difficulties  in  adult  and 

later  life,  142 
In  the   pulmonarj'   artcrv,  a  factor   in   the   causation  of   the    pulmonary 
systolic  murmur,  271,  555 
Case  where  this  was  the  main  factor,  (274).  300 
Blood  Volume  :  its  Compensatory  DimintjTion,  577 

In  deficiency  of  essential  constituents  of  the  blood,  163,  169 
In  starvation  in  enteric  fever,  168 
In  treatment  of  gastric  ulcer,  169 
In  hsemorrhage,  cholera,  &c.,  173 
In  neurasthenia,  &c.,  Ill 
In  heart  weakness  owing  to  the  heart's  inability  to  keep  the  normal  volume 
in  circulation,  54,  180,  185,  195,  578 
Its  occurrence  of  great  diagnostic  value  in  later  life,  94 
Clinical  e-sndences  of  its  compensatory  diminution,  579 
Rise  in  the  level  of  the  diaphragm,  163 
Hollowing  of  supra-clavicular  fossjc,  94,  134,  139 
Diminution  in  the  area  of  the  liver  dullness,  185 
Smallness  of  jugular  bulb  pulsation,  97,  133,  137,  583 
Emptiness  of  the  veins,  57,  61,  95,  132,  187 

Case  proving  the  compensatory  nature  of  the  emptiness  of  the  veins  in 
myocardial  weakness,  (140) 
Breathlessness : 

In  heart  failure  of  adolescence,  1 2 
In  the  right  ventricular  dilatation  of  anaemia,  228 
Its  cause,  245 

Characteristic  sighing  respirations,  13 
'  The  deep  breath,'  its  rationale,  15 
In  adult  life,  its  greater  importance,  36 
In  later  life,  diagnostic  difficulties,  113 
Bruit  de  diable: 

Due  to  constriction  of  dilated  veins,  15,  337 
Its  characters,  15,  337 

Its  variation  in  loudness  with  both  respiration  and  cardiac  action,  16 
Its  diminution  or  disappearance  with  the  recumbent  posture,  285,  337 
Bruit  de  galop  in  right  ventricular  dilatation,  due  to  the  occurrence  of  a  third 
sound,  340 


Calf  muscles,  pains  in  on  exertion,  a  sign  of  myocardial  weakness,  467,  470, 
(471) 
See  Leg  Pains 
Cardiac  cycle  consists  of  three  phases:  ventricular  contraction,  expansion,  and 
relaxation,  387 
Measurements  of  the  three  phases,  428 
See  Sounds  of  the  Heart 
Cardiac  dilatation,  see  Dilatation 


602  SUBJECT   INDEX 

Cardiac  dullness: 

Method  of  percussion,  20  to  25 

Its  shape  in  heart  failure  in  adolescence,  287 

adult  life,  40 
Its  increase  upwards  and  to  the  left  in  the  adolescent  type  of  right  ventricular 

dilatation,  25,  232 
Its  increase  on  lying  down  in  anremic  heart  failure,  266 
Its  diminution  or  absence,  a  sign  of  myocardial  weakness,  54,  5G,  (68) 
When  not  increased  in  heart  failure  the  cause  may  be  weak  muscle  or  abnor- 
mal rigidity  of  the  heart  wall,  34,  86,  91,  147 
Cardiac  failure  (.sec  Heart  Failure),  7 
Cardiac  impulse  (see  Apex  Beat) 

Its  character  in  adolescent  dilatation  of  the  right  ventricle,  17,  231,  331 
Diagnostic  value  of  impulse  in  outer  part  of  third  left  interspace,  19 

,,  ,,     at  sternal  end  of  fourth  left  interspace,  40 

If  weak  or  absent,  a  sign  of  myocardial  weakness,  60 

Its  disappearance,  after  being  abnormally  increased,  a  sign  of  improvement, 
„  ,,  „  ,,  a    sign  of   myocardial 

weakness,  (105) 
Cardiogram : 

Method  of  its  interpretation,  400,  494,  510 
In  aortic  regurgitation,  409 
„    mitral  „  403 

„       ,,       stenosis,  406 
Cardiographic  evidence  as  to  the  nature  of  the  expansion  phase  of  the  cardiac 
cycle,  400 
„  ,,        of  increased  aspiration  in  mitral  regurgitation,  403 

„  ,,  ,,  ,,  ,,         stenosis,  406 

„  ,,  ,,  lessened  aspiration  in  aortic  regurgitation,  409 

„  ,,         concerning  the  third  sound  of  the  heart,  427 

,,  ,,  ,,  mitral  mid- diastolic  murmur,  408 

Cardiographic   evidence   as  to   the  occurrence  of  ventricular  extra  systoles 

owing  to  mechanical  stimulation  of  the 
ventricle,  497 
„  „  ,.  tonic  and  contractUe  activity  of  the  walls 

of  the  auriculo-venous  reservoir,  500, 
504,  506 
„  ,,  of  value  in  the  diagnosis  of  aneurysm  of  the  trans- 

verse and  of  the  aorta,  215 
Cardiolysis  in  defective  compensatory  dilatation,  457 
Cardio-respiratory   murmur :     its   diagnosis  from  a  mitral  systolic  murmur, 

49,  446 
Classification  of  types  of  cardiac  failure,  6 
Coldness  on  exertion  a  sign  of  myocardial  weakness,  (365) 

,,  „         due  to  faulty  circulation  in  the  muscles,  472 

Collier,  Dr.  Mayo,  on  the  functions  of  the  auricles,  388 
Colon  dyspepsia  a  cause  of  palpitation,  119 

„  „  ,,  vasomotor  angina,  (127),  (130) 

„  ,,  „  local  asphyxia,  (128) 

„  ,,  simulated  by  pain  due  to  dilated  thigh  veins,  465 

Compensatory  phenomena  in  connection  with  the  heart  and  circulation,  see 

Summary,  p.  592 
Compensatory  diminution  in  the  volume  of    the    blood    in  circulation,  see 

Summary,  p.  577 
Compensatory  rise  in  the  diaphragm,  163 

,,  diminution  in  the  size  of  the  more  elastic  vascidar  viscera,  163, 

178 
.,  diminution  in  the  size  of  the  heart  in  myocardial  weakness,  50, 

186 


SUBJECT   INDEX  003 

Compensatory  emptiness  of  the  veins  in  heart  weakness,  case  proving  it,  (140) 
„  dilatation  of  the  left  ventricle  in  mitral  disease  by  means  of 

its  own  aspiratory  force,  397,  41G,  436 
Compensatory  character  of  muscular  cramp  for  improving  the  nutrition  of 

exhausted  muscles,  477 
Conductivitv  of  the  liver  tissue  to  percussion  vibrations,  pathological  variations 

in,  24,  l91 
Conus  arteriosus  of  the  right  ventriclo  : 
Its  distensibility  in  adolescence,  4,  9 

,,  ..  especially  in  ansemia,  228 

Cases  showing  dilatation  confined  to  it,  292,  (293).  (294) 
Extreme  strain  upon  the  conus  during  systole,  10 
Its  special  distensibility  lessened  in  adult  life.  31 
„  „  usually  lost  in  later  life,  32 

Cramp  on  exertion  a  sign  of  faulty  muscular  nutrition,  467,  471,  (477) 
Cyanosis,  37,  (469) 


Davies,  Dr.,  on  circulation  of  blood  through  diseased  hearts,  389,  451 
Deep  percussion  dullness,  see  Relative  Dullness,  21 

Diagnostic  Difficulties  : 

Connected  with  the  radial  pulse  in  adult  later  life.  35 

Case  where  a  normal  pulse  was  really  one  showing  heart  failure,  (35) 

The  interpretation  of  a  high  blood- pressure.     Is  it  too  high  ?     Is  it  normal 

for  the  patient  ?     Is  it  too  low  ? — 142 
False  and  true  venous  pulsation  in  the  neck  veins,  14,  39 
The  increase  and  decrease  of  pulsation  in  the  neck  veins  in  lieart  failure, 

table  of  phenomena,  137 
Dilatation  of  the  right  ventricle,  Essay  VII,  328 

Pulsation  in  the  second  left  interspace  and  aortic  aneurysm,  211,  (213) 
Pulmonary  systolic  and  aortic  systolic  murmur,  215 

„  „         „     tricuspid  systolic  murmur,  250,  279 

The  murmurs  due  to  tricuspid  regurgitation,  217 
The  tricuspid  systolic,  44,  217 
The  superior  vena  cava  murmur,  44,  218 
The  venous  valve  murmur,  219,  (291) 
The  arterial  compression  murmur,  226 
Aortic  systolic  murmur,  45 

„       regurgitant  murmur  when   there   is  a  mid-diastolic   addition  to  it 
simulating  a  true  Austin  FUnt  murmur,  394 
The  mitral  regurgitant  murmur.  48 

Estimation  of  the  amount  of  regurgitation  by  the  loudness  of  its  con- 
duction down  the  spine,  442 
And  cardio-respiratory  murmurs,  49,  446 
In  connection  with  the  recognition  of  heart  failure  in  later  life,  110 

Summary  of  opposing  statements,  160 
The  estimation  of  the  distensibility  of  the  heart  wall  in  later  life,  147 

Diagnosis  of  cardiac  enlargement  from  displacement,  151 
Displacement  downwards  simulating  enlargement,  (266),  (365) 
to  the  left  „  „  (374) 

Diagnostic  value  of  slight  lateral  displacement  of  the  heart  in  disease  of  the 

lung,  (375),  (376) 
Diagnostic  value  of  leg  pains  and  of  dvspnoea  respectivelv  in  cardiac  failure, 

469 
Diagnostic  difficulties  in  connection  with  pallor  and  anaemia  in  heart  disease, 
450,  453,  (454) 


Got  SUBJECT  INDEX 

Diagnostic  dillicultics  associated  with  the  recognition  of  referred  abdominal 
pain  due  to  dilatation  of  the  deep  veins  of  the  thigh,  (463),  465 

DiArHRAGM  : 

Its  normal  level,  163 

Its  degree  of  arching  determinable  by  percussion,  22,  165 

Its  elevation  by  pathological  changes  in  the  lung,  166,(167) 

„  ,,    diminution   in   the   amount   of    blood   circulating   in   the 

thoracic  viscera,  261,  580 
In  malnutrition  :  in  enteric  fever,  168 
,,  in  gastric  ulcer,  171 

In   cardiac  weakness,  57,  180 
In  neurasthenia,  &c.,  177 
Low  in  emphysema,  362 

„    in  pleuritic  effusion,  &c.,  363 

,,    in  chronic  venous  congestion  in  valvular  disease,  &c.,  (318),  363,  (365), 
(366),  591 
Diastolic  wave  in  the  neck  veins,  a  sign  of  rigidity  of  the  right  ventricle,  398 


Dilatation  of  the  Heart  and  Veins 
Theory  of  dilatation  of  the   ventricles  when   over-strained  in  any  way,  6, 

9,  31,  211 
Factors  which  determine  the  typo  and  the  amount  of  dilatation,  542 
Various  types  of  dilatation,  543 

Adult  and  adolescent  types  of  dilatation  compared,  5,  10,  31,  330 
Relative  liability  to  dilatation  of  the  right  and  left  ventricles  respectively 
at  different  periods  of  life,  10,  31,  46,  309 
with  different  kinds  of  exertion,  308 
Of  the  right  ventricle,  329 

Upwards  and  to  the  left  in  adolescence,  4,  10,  25,  228 
CUnical  aspects  of,  14,  228,  330 
Early  recognition  of,  28 
Various  types  of,  in  anseraia,  289 

Its  relationship  to  the  pulmonary  artery  murmur,  264 
Characteristic  form  of  dilatation  in  overstrain,  309 
Cases  showing  great  dilatation,  (235),  (304) 
To  the  right  in  adult  life,  37 

Lessened  frequency  of  dilatation  in  later  life,  5,  73,  79 
Left  ventricle  less  liable  to  be  affected  by  overstrain  in  adolescence  than  in 

adult  life,  46,  308 
In  compensation  for  valvular  disease,  see  also  Ventricle,  Left,  397 
Of  the  right   auricle   (see  also  Auricle),  41 

Of  the  superior  vena  cava,  a  cause  of  a  murmur,  44,  218,  (224),  (280) 
Cases  showing  extreme  dilatation  of  the  heart : 
Cases  in  adolescence,  (7),  (277),  (281),  (304),  (314) 
„      „  later  life,  (320) 
,,      of  the  left  auricle,  (455) 
„  ,,      right  auricle,  (236) 

Does  not  occur  in  great  myocardial  weakness,  6 
Dilatation  of  a  weak  heart  a  sign  of  returning  strength,  63,  (102),  (294),  (304), 

(316),  570 
Dilatation  of  the  heart  simulated  by  displacement : 

1.  Downwards,  owing  to  lowness  of  the  diaphragm,  362 
In  emphysema,  362 

In  chronic  venous  congestion  of  the  lungs,  363,  (364),  (366) 

2.  Downwards,  owing  to  elongation  of  the  first  part  of  the  aorta  in  aortic 

regurgitation,  346 

3.  To  the  left,  in  collapse  of  llie  left  lung,  (374) 


SUBJECT  INDEX  605 

Displacement  of  tue  Heart,  Essay,  345 

The  relative  mobility  of  the  heart,  especially  in  adolescence,  (371),  (377) 
Rapidly  developed  displacement  from  collapse  of  lung,  (371) 
Mobility  of  the  tissues  forming  the  posterior  mediastinum,  379 
The  fixation  points  of  the  heart  are  only  relatively  '  fixed,'  371 
The  main  fixation  points,  379 

Inferior  cava  where  it  passes  through  the  diaphragm  an  important  one, 

380 
Their  bearing  upon  displacements  in  general,  379 

„  „  upward  displacement  of  the  apex,  3oS 

„  „  rotation  of  tlic   heart  in  displacement  to   the  right, 

379 
„  .,  the  rotation  of  the  right  auricle  towards  the  anterior 

chest  wall,  (381) 
„  „  rotation  of  the  heart   in  displacement  to   the   left, 

383 
Altered  relationships  of  a  displaced  heart,  379 
Murmurs  due  to  cardiac  displacement,  383 
Causes  of  displacement  may  be  intrinsic  or  extrinsic,  345 
Intrinsic  causes — 
Aneurysm,  345 

Intrapericardial  aneurysm,  (395) 

Aortic  regurgitation  a  cause  of  downward  displacement,  346 
Upward  displacement  of  apex  due  to  downward  enlargement  of  right  ventricle 
348 
„  „  due  to  adolescent  dilatation  of  the  right  ventricle,  348 

„  „  „     „  „  „      See  Apex 

Extrinsic  causes  of  displacement  of  the  heart,  361 
Forwards,  361 
Backwards,  361 

Downwards,  due  to  lowness  of  diaphragm,  362 
Effusion  of  Uquids  into  pleura,  362 
Over-distension  of  lungs  with  air,  362 
Over-distension  of  thoracic  vessels  with  blood,  363 

In  '  chronic  venous  congestion,'  (318),  (364),  (366) 
Growth  of  tumours  in  the  thorax,  (379) 
Upward  displacement,  368 
By  adhesions,  371 

By  excess  of  abdominal  pressure,  ascites,  &c.,  368 

By   traction   owing   to   diminution   in  the  size  of  the  thoracic  viscera, 
368 
In  pulmonary  fibrosis  in  phthisis,  &c.,  (167) 
In  compensatory  diminution  in  the    volume    of    blood  in  circulation, 

in  defective  nutrition,  &c.,  168,  368,  (370) 
In  heart  weakness,  180,  (368) 
Lateral  displacement,  371 

Diagnostic  value  of  small  amount  of  lateral  displacement,  375,  (376) 
To  the  left,  (371),  373 

„         ,,   simulating  enlargement  of  the  heart,  (374) 
To  the  right,  377 

An  extreme  case,  (377) 

Case  due  to  cancer  of  lung,  (379) 

DiSTENSiBiLiTY  OF  THE  Heart  Wall,  See  Summary,  pp.  533  to  541 
Variation  in  the  heart's  distensibility  with  age,  535 
Great  in  adolescence,  5,  7,  9 
Lessening  as  age  advances,  6,  10,  33 
Practically  lost  sometimes  in  later  life,  6,  79,  81,  85 


606  SUBJECT  INDEX 

DiSTENsiBiLiTY  oii"  THE  Heart  Wall  {co7itinued) : 
Local  variation  in  distensibility — 
Great  in  adolescence,  8 
Local  variations  in  the  distensibility  of  the  walls  of  the  right  ventricle, 

4,  9 
Right  ventricle  more  distensible  than  the  left,  11 
In  adult  hfe  local  variations  in  distensibihty  are  less,  5,  11,  31,  309 
„       „      „    left  ventricle  as  dilatable  as  the  right,  31 
In  relation  to  heart  failure  without  enlargement,  6,  50,  86,  91,  537 
Its  clinical  estimation,  539 
Simple  in  adolescence,  54 
In  .adult  life  often  not  easy,  34 
In  later  life  often  extremely  difficult,  147 
Dropsy,  not  a  sign  of  myocardial  weakness,  94 
Dullness,  see  Absolute,  Relative,  Cardiac  Dullness,  and  Liver  Dullness 

Elasticity  of  the  heart  wall,  see  Distensibihty,  7 
Elastic  thigh- supports  for  the  cure  of  dilated  deep  thigh- veins,  466 
Enlargement  of  the  heart,  see  Dilatation  and  Heart  Failure 
Enteric  fever,  pulse  characteristic  of  heart  weakness  in,  59 

„        „      diminution  of  blood  volume  in,  168 

„         „      wliere  percussion  dullness  did  not  indicate  the  true  size  of  an 
enlarged  Uver,  153 
E?:pansile  force  of  the  blood  aspirated  by  the  left   ventricle  shown  by  the 

cardiograph,  436 
Expansile  tone  of  the  colon,  a  cause  of  vasomotor  angina,  (127) 

Expansion  Phase  of  the  Cardiac  Cycle,  384,  400 

The  ventricles  enlarge  suddenly  after  contraction  in  virtue  of  an  active  e;xpan- 

sion  of  the  muscular  fibres,  384,  400 
This  expansion  is  due  probably  to  a  transverse  contraction  of  the  sliortened 

fibres  causing  them  to  lengthen,  384,  400 
The  heart  muscle  is  known  to  remain  hard  for  an  appreciable  time  after  the 

closure  of  the  semilunar  valves,  385,  401 
The  cardiograph  shows  the  ventricle  to  be  enlarging  immediately  after  the 

closure  of  the  semilunar  valves,  385,  403,  521 
An  expansion  phase  must  be  recognised  in  the  cardiac  cycle,  386,  428 
Three  phases  of  the  cycle  :   contraction,  expansion,  relaxation,  387 
It  lasts  one-tenth  of  a  second,  386,  428 

Its  duration  does  not  vary  materially  as  is  the  case  with  contraction,  387 
The  duration  of  the  expansion  phase  is  adequate  for  the  complete  emptying 
of  the  auricle  into  the  ventricle,  387 
The  ventricle  is  therefore  a  double-acting  pump,  filling  itself  with  its  own  back 

stroke,  384,  400 

The  recognition  of  a  muscular  expansion  phase  explains  the  compensatory 

phenomena  of  valvular  disease  {vide  Summary,  Compensatory  Phenomena. 

592),  412 

It  explains  the  compensatory  underfilling  of  a  heart  that  is  musculaiiy  weak,  52 

It  explains  the  diminution  in  the  size  of  the  heart  which  characterises  severe 

myocarditis  when  occurring  in  a  '  distensible  '  heart,  53 
Feeble  muscular  aspiration  accounts  for  the  compensatory  diminution  in  the 
blood  volume  which  is  observable  in  myocardial  weakness,  52,  80 

Extra  systoles,  due  to  mechanical  stimulation  of  the  ventricle,  495,  497 

Fatty  degeneration  of  the  right  ventricle  with  a  fairly  strong  left  ventricle, 

(154),  (156) 
Fatty  degeration,  see  Myocardial  Weakness 


SUBJECT  INDEX  607 

Fibrous  Tissues  : 

Thoir  immaturity  in  adolescence  deprives  the  heart  ot  any  support  they 

might  give,  5,  10 
In  adolescence  the  resisting  power  of  the  heart  wall  depends  mainly  upon 

its  muscular  strength,  9 
The  heart  in  adolescence  is  very  distensible,  and  increases  or  diminishes  readily 
in  size,  8,  53 
In  adolescence,  compensatory  underfilling  of  the  ventricle  in  myocardial 
weakness  takes  place  readily,  54 
Their  immaturity  also  allows  changes  in  the  size  or  position  of  organs  to 
take  place  readily,  72 
Diaphragm  rises  readily  when  bulk  of  thoracic  contents  is  diminished,  94 
Displacement  of  the  heart  takes  place  readily  in  diseases  of  the  lung  or 
pleura,  (371) 
Their  increasing  strength  as  age  advances  gives  support  to  the  heart  wall, 

51,  53 
In  adult  and  later  Ufe  dilatation  takes  place  less  readily  than  is  the  case 

earUer  in  life,  31,  79 
In  later  life  tliis  change  may  amount  to  what  is  practically  a  fibroid  degenera- 
tion of  the  heart  wall  itself,  5,  78 
Tills  increase  in  the  resisting  power  of  the  heart  waU  ensures  its  possession 
of  mechanical  elastic  recoil  after  contraction  in  addition  to  its  muscular 
expansile  power,  53,  80 
This  change  lessens  or  prevents  compensatory  diminution  in  the  size  of 

the  full  ventricle  in  myocardial  weakness,  80 
It  lessens,  but  does  not  prevent  compensatory  diminution  in  the  volume 
of  blood  in  circulation  in  myocardial  weakness,  in  adult  and  later 
Ufe,  80 
It  renders  the  occrn'rence  of  angina  pectoris  and  of  deatli  from  asystole 
possible  in  adult  and  later  life,  54,  82 
Increased  resisting  power  of  fibrous  tissues  makes  changes  in  the  size  and 
position  of  organs  take  place  less  readily,  72,  76,  94 
Changes  in  the  level  of  the  diaphragm  take  place  less  readily  and  are  less 
extreme  in  adult  and  later  life  than  in  adolescence,  72 

'  The  fidgets  ' :   restlessness  caused  by  dilatation  of  the  deep  thigh- veins,  462 
Filling  of  the  ventricle,  compensatorily  lessened  in  extreme  muscular  weakness 
in  distensible  hearts,  53 

Compensatory   underfilling    less   complete   when   the   heart   walls   possess 
mechanical  elastic  recoil,  80 
Fixation  points  of  the  heart,  see  Displacement  of  Heart 
FoxweU,  Dr.,  on  Ansemic  Heart  Failure,  234 
'  Functional '  heart  murmurs  : 

Pulmonary  systolic,  254 

Mitral  systolic,  48,  (281) 

Mitral  mid-diastolic  mmunur,  (286) 

Tricuspid  regurgitation,  43,  279 

Tricuspid  mid-diastolic  murmur,  46,  282 


Gastkic  resonance,  as  an  indication  of  the  level  of  tlie  diaphragm,  164 

Variations  in  its  level  of  great  diagnostic  value  in  cases  of  myocardial  weak- 
ness, 57,  94,  180. 
Reverberation  as  a  method  of  its  detection,  480 
Gastric  ulcer  with  extreme  diminution  of  blood- volume  and  small  liver  dullness, 

(171) 
Dr.  Lockhart  Gibson  on  the  mitral  mid-diastoUc  murmur,  384,  400 
'  Globus  hystericus,'  in  dilatation  of  the  right  ventricle,  14,  (212),  342 


608  SUBJECT  INDEX 

Habit  palpitation   after   severe  myocardial   weakness ;    after   influenza  and 

diphtheria,  117,  (119) 
Habit   sluggishness   of   the  vasomotor   mechanism,  a  cause   of   intermittent 

claudication,  475,  (-176) 
Habit  tachycardia  after  overstrain,  (324) 
Haemorrhage  causing  high  diaphragm,  (176) 

„  „        small  liver  dullness,  (203) 

Haemic  murmur  of  anaemia,  see  Pulmonary  Systolic  Murmur 
Haemic   murmur  in   the  neck,   see   '  Bruit  de  diable,'   Superior   Vena   Cava 

Murmur,  Arterial  Compression  Murmurs,  and  Venous  Valve  Murmur 

Heart  Failure,  definition  of  term,  1 
With  enlargement,  542 

In  the  distensible  heart  of  adolescence,  12 

In  the  moderately  distensible  heart  of  adult  life,  35 

In  the  relatively  rigid  heart  of  later  life,  70,  571 

In  anaemia,  227 

In  overstrain,  308 
Without  enlargement,  50,  85,  564 

In  the  distensible  heart  of  adolescence,  53,  565,  567 

In  heart  failure  with  small  heart,  54 

In  the  moderately  distensible  heart  of  adult  life,  53,  566,  569 

In  moderately  strong  but  relatively  rigid  hearts,  73,  86,  (87),  (89) 

In  weak  and  relatively  rigid  hearts,  91 

CompUcating  pneumonia,  (97) 

But  accompanied  by  signs  of  a  normal  heart  and  normal  circulation,  149 
Heart  sounds,  their  measured  loudness  in  health  and  disease,  420-426 
Method  of  measuring  their  loudness,  413 
See  Sounds  of  the  Heart 
Heart  wall,  elasticity  of,  7 

„         „      distensibility  of,  see  Distensibility,  and  Summary,  533 
„         „      relatively  rigid  in  later  life,  5,  76 
High  diaphragm  a  sign  of    compensatory  diminution  in  the  blood  volume, 
163,  580 

Impulse  of  heart,  see  Cardiac  Impulse 
Intermittent  claudication,  471 

A  sign  of  myocardial  weakness,  92,  469 
Due  to  vasomotor  disturbance,  472 

Due  to  habit  sluggishness  of  the  vaso-dilator  mechanism,  (476) 
Cured  by  brisk  e^cercise,  477 
Interventricular  septum,  part  played  by  it  in  the  causation  of  the  raised  apex 
beat  in  adolescent  dilatation  of  the  right  ventricle, 
237,  359 
„  „         its  position  shown  on  the  chest  by  the  limitation  of 

the   area   of  audition  of  the   third  sound  to  the 
ventricle  in  which  it  arises,  (284) 
Intraventricular  pressure  must  be  the  agent  causing  dilatation  of  the  heart,  6,  31 
„  „       a  high  pressure  necessary  for  causing  upward  dilatation 

of  the  right  ventricle  in  adolescence,  239 

Jugular  Bulb,  palpation  of,  its  clinical  value,  133,  583,  590 

Later  life,  early  diagnosis  of  heart  failure  in,  70.  571 

Left  Ventricle  (see  also  Ventricles),  561 

Dilatation    and   hypertrophy   necessitated    by    compensation    for    valvular 

leakage,  47,  389 
Dilatation  in  mitral  incompetence  brought  about   by  increased   aspiratory 

force,  397 


SUBJECT  INDEX  609 

Left  Ventricle  {continued)  -. 

Hypertrophy   in   mitral   stenosis    sometimes   accompanies   its   increased 

aspiratory  activity,  391,  418 
Inadequate  compensatory  dilatation  a  sign  of  («)  abnormal  rigidity  of  its 

walls;    {b)  weakness  of  its  muscle,  (65),  150 
Diminution   in   the   amount  of    compensatory   dilatation   a  sif:^   of  tho 

onset  of  myocardial  weakness,  (112),  (310) 
In  overstrain  in  adolescence,  11,  309 

Dilatation  often  prevented  by  the  prior  failure  of  tho  right  ventricle,  47, 309 
Sometimes  dilatation  well  marked,  (277),  (281) 
In  adult  life  dilatation  of  tho  left  ventricle  equals  or  exceeds,  in  frequence, 

that  of  the  right,  46,  316 
Case  of  extreme  dilatation,  (320) 
Leg  Pains  of  CracuiiATORY  Origin,  459 

Due  to  LOC^VL  abnormality  in  the  circulation — 
Due  to  dilatation  of  the  deep  thigh-veins,  459 
Probable  pathology,  pressure  on  nerves,  460 

Occurrence  of  pain  on  standing  or  in  the  evening  is  characteristic,  461 
Nature  of  discomfort  sometimes  indescribable,  462 
Pain  often  referred  or  segmental  in  character,  462 
Sometimes  localised  in  groin  and  simulating  colon  dyspepsia,  465 

,,  only  a  remote  effect  on  nervous   system  and  a  potent  cause 

of  neurasthenia,  462 
'  The  fidgets,'  if  coming  on  in  the 'evening,  a  characteristic  result  of  dilated 

deep  thigh-veins,  463 
Referred  hip-pain  simidating  neuralgia,  (463) 
Easily  cured  by  elastic  support  to  the  thigh,  (464),  466 
A  simple  support  made  from  elastic  webbing  bandage,  46() 
Neurasthenia  cured  liy  elastic  thigh-supports,  (464),  (465) 
Due  to  deficient  blood  supply  to  the  muscles,  467 
Intermittent  claudication,  471 

„  „  due  to  vasomotor  disturbance,  472,  (473)  ■ 

„  „  due     to     habit    sluggishness     of     vaso-dilator 

mechanism,  475,  (476) 
„  cured  by  brisk  exercises,  (474),  (476) 

Leg  pains  due  to  deficiency  of  the  general  circulation,  owing  to  heart  weakness, 
467,  469 
In  muscular  weakness  from  malnutrition  the  calf  muscles  are  the  first  to 

suffer,  468 
Pain  in  calf  muscles  due  to  transient  heart  weakness,  (468) 

„  „  a  valuable  sign  of  myocardial  degeneration,  92,  468 

Diagnostic  value  of  pains  in  the  calf  muscles  and  of  dyspnoea  respectively  in 

heart  failure,  470,  (471) 
Coldness  on   exertion   a  sign   of    defective    muscular  nutrition  and   often 

associated  with  leg  pains,  (365),  (474),  (475) 
Cramp  on  exertion  due  to  faulty  nutrition  of  the  muscles,  472,  (477) 

Liver 
Jlethod  of  its  percussion,  21,  189 
Normal  level  of  the  upper  border  of  its  dullness.  165 
Variability  of  the  lower  edge  of  its  dullness,  165 
Causes  of  variation  in  its  area  of  dullness,  189,  581 

1.  Its  tissue  when  abnormaU}'  tense  or  abnormally  flaccid  appears  to  some 

extent  to  lose  its  power  of  masking  the  resonance  of  underlying  organs, 

24,  191 

In  an  enlarged  and  congested  liver  the  absolute  dullness  does  not  come 

down  as  near  to  the  edge  of  the  liver  as  would  be  the  case  in  a  normal 

organ,  24,  191 

2  B 


610  SUBJECT  INDEX 

Liver  (continued) : 

Case  of  enlarged  liver  in  enteric  fever  where  the  lower  border  of  absolute 
dullness  was  three  inches  away  from  the  edge  of  the  liver,  153 
When  less  distended  with  blood  than  normal  there  is  also  increased  con- 
ductivity to  percussion  vibrations  causing  a  diminution  of  the  liver 
dullness,  24,  191 
In  cardiac  weakness  this  diminution  varies  with  the  strength  of  the  heart, 

so  exactly  as  to  suggest  a  close  connection,  193 
Diminished  liver  dullness  a  sign  of  myocardial  weakness,  58,  95,  185,  &c. 

2.  Liver  dullness  may  also  be  lessened  by  the  drawing  up  of  the  liver  under 

an  abnormally  high  diaphragm,  165,  190 
Rise  in  the  lower  edge  of  the  liver  dullness  in  a  rise  in  the  diaphragm  owing 
to  the  absorption  of  pleuritic  effusion,  (103) 

3.  Diminution  in  the  area  of  liver  dullness  owing  to  undue  flaccidity  allowing 

it  to  fall  away  from  the  anterior  abdominal  wall  and  the  ribs,  58,  190 
Case  proving  this,  (205) 

4.  Actual  shrinkage  in  size  when  underfilled  with  blood,  must  play  some  part 

in  causing  a  lessening  of  its  dullness,  188,  189 
Diminution  in  the  size  of  the  liver  dullness  due  to  other  causes  than  heart 

failure  (see  Summary,  p.  578),   152,  202 
Diminution  in  the  size  of  a  liver  enlarged  by  chronic  venous  congestion 

a  sign  of  myocardial  weakness  and  not  of  a  gain  in  strength,  (63) 

Local  asphyxia  and  syncope  of  the  fingers  a  reflex  result  of  irritation  of  an  irrit- 
able colon,  (128) 

Long  breath  in  dilatation  of  the  right  ventricle,  12 

Loudness  of  the  heart-sounds,  measurement  of  the,  413 

„        of    right   ventricular    sounds   in   absolute   and   relative   overstrain 
respectively,  29 

Lungs,  diminution  in  the  size  of  the  healthy  lung  in  pneumonia,  a  sign  of 
dangerous  myocardial  weakness,  97 


Mechanical  elastic  recoil  possessed  by  the  heart  wall  in  adult  and  later  life, 
79 
Its  presence  lessens  or  prevents  compensatory  diminution  in  the  size  of  the 

heart  in  myocardial  weakness,  53,  80 
Lessens  but  does  not  prevent  compensatory   diminution  in   the  volume  of 

blood  in  circulation,  81 
Renders    the    occurrence    of    anginal    pain    and    of    death   from    asystole 
possible,  53,  81 
'  Meniere's   disease,'  symptoms  of,  simulating  heart  failure,  121 

,,  „        hypersesthesia  of  semicircular  canals,  a  valuable   sign  of, 

123 
Micturition  :    danger  of  adopting  erect  attitude  when  heart  is  muscularly  weak, 
126 
„  rationale    of    the    squatting    attitude    adopted    by    natives  of 

India,   126 
MiD-DiASTOLic  Mttrmur,  393,  408 

A  '  Relaxation,'  miirmur  occurring  at  the  commencement  of  the  relaxation 

phase,  293,  408 
It  occurs  therefore  at  the  end  of  the  expansion  phase  one-tenth  of  a  second 

after  the  second  sound,  394,  408 
It  is  produced   by  the  aspiratory  force  developed  during  the  expansion 

phase,  393 
It  is  due  to  the  vibration  of  the  segments  of  the  mitral  valve  in  the  blood 

stream  flowing  from  the  auricle  into  the  ventricle,  393,  408 
The  valve  flaps  are  only  free  to  vibrate  on  the  relaxation  of  the  musculi 
papillares,  393,  408 


SUBJECT  INDEX  ^11 

MiD-DiASTOLic  MuKMUR  (continued) : 

The  mid-diastolic  murmur  can  only  occur  when  the  flow  from  the  auricle 

into  the  ventricle  is  prolonged  until  the  commencement  of  the  relaxation 

phase,  431 
Causes  of  prolongation  are  : 

1.  Stenosis  of  the  auriculo-ventricular  orifice,  394,  431 

2.  Dilatation  of  the  auricle  to  a  greater  extent  than  the  ventricle,  435 

3.  Slight  lessening  of  the  aspiratory  force  through  muscular  malnutrition, 

as  in  anaemia,  282 
Mitral  mid-diastolic  of  functional  origin,  (286) 
Tricuspid  „  „  „         (289),  341 

Mid-diastolic  addition  to  the  aortic  regurgitant  murmur  can  be  caused  in  the 
same  manner,  but  by  the  regurgitating  blood  flowing  over  the  anterior 
aspect  of  the  anterior  mitral  cusp,  394 
Mitral  regurgitation,  process  of  compensation  in,  389,  403,  416,  594 
Mitral  stenosis,  process  of  compensation  in,  390,  406,  418,  595 
Mitral  systolic  murmur : 

The  first  reliable  sign  of  left  ventricular  failure,  48 
Diagnosis  from  a  tricuspid  systolic,  48,  217 

„  „       cardio-respiratory  murmur,  49,  446 

Diagnostic  and  prognostic  importance  of  noting  the  loudness  of  its  conduction 

down  the  spine,  442 
Reasons  for  its  conduction  to  the  angle  of  the  scapula,  442 
Absent  in  spite  of  extreme  dilatation  of  the  left  ventricle,  (281),  (320) 
Mitral  valve : 

Its  segments  held  rigid  during  the  expansion  phase ;    therefore  no  vibration 

of  them  possible  before  the  onset  of  relaxation,  393,  431 
No  flow  of  blood  through  the  valve  in  normal  heart  after  the  end  of  the 
expansion  phase,  and  therefore  there  is  no  sound  in  the  normal  heart 
at  the  onset  of  relaxation,  393,  430 
See  also  Mid-diastolic  Murmur,  Mitral  Regurgitation,  Mitral  Stenosis 
Muscular  cramp  :    a  compensator}'^  phenomenon  tf)  improve  the  nutrition  of 

exhausted   muscles,  (477) 
[Muscular  expansion  of  the  heart  {see  Expansion)  in  relation  to  compensation 
for  valvular  disease,  vide  Essays  IX,  X,  XI,  and  XII,  and  Summary,  p.  594 
In  relation  to  compensatory  diminution  in  the  size  of  the  heart,  52 
Develops  the  force  whereb^^  compensatory  dilatation  of  the  left  ventricle  is 
brought  about  in  mitral  regurgitation,  397,  436 
Muscular  strength  of  the  heart  wall  is  the  main  factor  in  resisting  dilatation  in 
adolescence,  4,  8,  9,  31 
Difficulty  in  distinguishing  between  muscular  and  fibrous  strength  of  the 
heart  wall  in  later  life,  34,  85,  147 
Myocardial  weakness,  signs  of  : 

In  adolescence,  diminution  or  disappearance  of  cardiac  dullness,  56,  60,  96 
Feebleness  of  cardiac  impulse,  56,  96 
Characteristic  pulse,  35,  56,  59,  95 
High  diaphragm,  57,  163 
Small  liver  dullness,  185 
In  adult  and  later  life,  94 

Compensatorv  diminution  in  size  of  heart  less  marked  as  age  advances, 

72,  79 
Changes  in  level  of  diaphragm  leas  extreme,  72,  94 
Rise  in  the  level  of  the  gastric  resonance  of  value,  94 
Diminution  of  the  area  of  liver  dullness  of  value,  95 
Signs  of  compensator}'  diminution  of  the  blood  volume  given  by  (a)  hoUow- 

ness  above  the  clavicles,  94 
(b)  By  emptiness  of  the  venous  system,  95 
Signs  of  myocardial  weakness  given  by  variation  in  the  amount  of  pulsation 
in  the  neck  veins,*  132,  137 


012  SUBJECT  INDEX 

Nbok  veins  :  diagnostic  value  of  phenomena  connected  with  them,  132,  137 

See  Veins 
Neuralgia  of  the  hip  simulated  by  dilated  deep  thigh-veins,  (463) 
Neurasthenia  duo  to  dilated  deep  thigh- veins  cured  by  elastic  thigh-supports, 

462,  466 
Nitroglycerine:  its  action  in  vasomotor  angina  due  to  colon  dyspepsia,  (130) 
„  causes  a  'filling-up  of  the  veins  when  there  is  compensatory 

emptiness   of  them,  (140) 
,,  cautions  as  to  its  use  in  weak  and  '  rigid  '   hearts,   148 

Nocturnal  occurrence  of  attacks  of  palpitation  or  of  angina  pectoris  suggests 

their  reflex  colon  origin,  (116),  (131) 
Nutrition  of  the  heart,  its  importance  in  cardiac  failure,  5,  449 

,,  „  a  factor  in  the  heart  failure  of  anaemia,  242 

Optic  neuritis  in  anaemia,  (297) 
Overaction  of  right  ventricle: 
iSigns  of  in  adolescence,  4,  12,  82 
„     adult  life,  40 
„         „     vahailar  disease  in  relation  to  compensation,  414 
Of  great  value  in  estimating   the   amount   of   cardiac   rigidity  present  [in 
heart  failure  in  later  life,"(87),  (89) 
Over-exertion,  a  factor  in  the  cardiac  dilatation  of  anaemia,  247,  (303) 
Over-stimulation  of  the  heart:  a  danger  to  be  avoided  in  myocardial  weakness,!  11 

Overstrain  of  the  Heart,  308 

Apportionment  of  strain  on  right  and  left  ^■entricles,  10,  46,  309,  545 
Definition  of  terms  '  Relative,'  and  '  Absolute,'  310,  342 
Conditions  causing  overstrain,  545 

Overstrain  in  adolescence,  (212),  (310),  (312).  (313) 
in  adult  Ufe,  316 
„  in  young  man  with  unusual  symptoms,  and  result,  (324) 

„  due  to  the  sudden  cessation  of  severe  exertion,  327 

in  later  life  (83),  (320) 
„  ,.  before  estimating  its  amount,  allowance  to  be  made 

for  degree  of  rigidity  of  the  heart-wall,  86,  147 
Overstrain  of  the  right  ventricle  the  result  of  valvular  disease,  (339),  (435), 

(455),  &c. 
Overstrain   an   important   factor  in   the   causation    of   the   heart    failure  of 

anaemia,  244 
Overstrain  of  the  left  ventricle  in  adolescence,  (281) 

Pain  in  the  groin,  due  to  dilated  deep  thigh-veins,  465 

.,     in  the  legs,  of  circulatory  origin  (sec  Leg  Pains,)  459 

„     in  upward  dilatation  of  the  right  ventricle,  36,  (212),  (313) 

..     anginal  pain,  see  Angina  Pectoris 
Pallor  and  anaemia,  definition  of  terms,  448,  450 

In  transient  heart  weakness,  450 

In  serious  heart  weakness,  451 

Due  to  deficiency  in  the  circulating  blood  in  faulty  compensation,  452 

In  aortic  regurgitation,  452 

In  mitral  regurgitation  (454) 

Liability  of  mistaking  pallor  due  to  faulty  compensation  for  anaemia,  453, 
(456) 

Due  to  undue  rigidity  of  the  heart-wall  interfering  with  compensatorv  dilata- 
tion, 454,  (455),  (456) 

Prognosis  in,  457 

Risk  of  sudden  death  in  patients  with  pallor,  458 


SUBJECT  INDEX  613 

Palpitation,  114 

„  as  a  cardiac  habit,  117 

„  when    nocturnal   its   reflex    origin    in    the   colon   is   suggested, 

(116) 
Pathological  facts  in  connection  witli  dilatation  of  the  right  ventricle,  233, 
247 

Percussion  of  the  Heart,  method,  20 

Nomenclature.     Tlie  terms  'relative'  and  'alisolutc'  dullness  preferal)lo  to 

'  sup(;rficial  '  and  '  deep,'  21 
Value  of  firm  and  light  percussion,  20,  22,  24 
ISupposed  unreliability  of  relative  dullness,   20 
Confirmation  of  relative  dullness  by  percussing  again  with  tiic  lungs  emptied, 

22 

Percussion  of  the  Liver,  22,  189 

Degree  of  arching  of  diaphragm  sliown  ))y  percussion  of  its  upper  border, 

23 
Percussion  of  its  lower  border  usually  neglected,  23 
Uncertainties  associated  with  its  percussion,  24 

Diminution  in  the  area  of  absolute  liver  dullness  due  to  changes  in  the  con- 
ductivity of  the  liver  tissue  to  percussion  vibrations,  191 
Increased  conductivity  due  to  the  increased  tension  which  results  from  over- 
distension with  blood,  24,  153 
Increased  conductivity  also  probably  due  to  the  lessened  tension  which 
results  from  relative  emptiness  of  its  blood-vessels,   191 
Generalisation  as  to  firm  and  gentle  percussion  when  a  solid  organ  is  overkiid 

or  underlaid  by  a  resonant  one,  23 
Points  to  bo  noted  in  percussion  of  the  sternum,  25 
I'ericai'dium  : 

Its  power  of  limiting  cardiac  dilatation,  slight  in  adolescence,  increasing 

witli  age,  5,  11 
Its    relationship    to    the    superior    vena    cava,  giving  rise  to  the    superior 
vena  cava  murmur,  44 
I'hear,  Dr.  A.,  on  the  third  sounil  of  tlie  heart,  427 
I'liysical  signs  of  heart  failure  :    their  aburncc  in  ])neumoiiia,  ito.,  may  show 

dangerous  heart  weakness,  (97),  (105) 
Pneumonia,  accompanied  by  a  rapid  dilatation  of  tlie  light  ventricle  and  a 
rise  in  the  ape;s  beat,  (3(50) 

High  diaphragm  in,  showing  myocardial  weakness,  (97),  (224) 
Interpretation  of  phenomena  due  to  cardiac  weakness,  98,  105 
Pneumococcal  toxin,  causing  a  rise  in  the  blood  pressure,  103 
Position,  change  of,  affecting  : 

Amount  of  upward  dilatation  of  the  right  ventricle,  266 
*  Bruit  de  Diable,'  16 
Mid-diastolic  murmur,  (284) 

Pulmonary  artery  systolic  murmur,  256,  266,  300 
Tricuspid  third  sound,  (313) 

Tricuspid  systolic  murmur,  lessened,  201,  (284),  303 
„  ,,  „  no  change,  (301) 

Presystolic  murmur : 

A  spurious,  due,  in   a  rai)id  ))eat,  to  tlie  approximation   of  a  mid-diastolie 
aortic  murmur  to  the  following  tu'st  sound,  394 
Pulmonary  artery  systolic  murmur,  254  :  see  Summary,  p.  551 
Pulmonary   artery :    its    altered   relationships   in   upward   dilatation   of   the 

right  ventricle,  251 
Pulmonary  orifice  :    its  dilatation  a  cause  of  the  absence  of  the   pulmonary 
systolic  murmur  in  great  upward  dilatation  of  the  right  ventricle,  271, 
(294),  &c.,  556 


614  SUBJECT  INDEX 

I'lilsatiou : 

In  upward  dilatation  of  thu  right  vcnlrick'  its  special  characters,  17  j 
Diagnostic  value  of  pulsation  in  the  outer  part  of  the  third  left  interspace,  19 
Diagnostic  ■value  of  pulsation  at  sternal  end  of  fourtli  and  fifth  left  inter- 
spaces, 29,  40 
Pulsation  in  the  jugular  bulb  :  its  importance,  133 

„  ,,      neck  veins :  diagnostic  significance  of  it,  137 

To  the  right  of  the  sternum,  usually  due  to  the  right  ventricle  not  to  the 
auricle,  41 
Pulse,  radial :    characteristic  of  extreme  heart  weakness,  59 
Collapsing  in  fatty  right  ventricle  with  strong  left,  (155),  159 
May  be  an  uncertain  guide  in  adult  and  later  life,  35,  143 
Pulse,  venous  :  felt  in  jugular  bulb  behind  clavicle,  133 


Rabagliate,  Dr.,  on  muscular  pains  and  tenderness,  478 
Reduplication  of  the  heart  sounds,  see  Sounds  of  the  Heart 

,,  spurious,  of  the  first  sound    may  be  due  in  a  rapid  heart  to 

approximation  of   a   third    sound    to    the   succeeding   first 
sound,  vide  p.  394 
,,  spurious,  of  second  sound  at  the  apex,  see  Third  Sound 

Referred  pain  in  dilatation  of  the  deep  thigh-veins,  462 
Relative  percussion  dullness,  see  Percussion,  21 

,,         overstrain,  as  distinct  from  '  absolute,'  310,  343 
Reservoirs : 

Auriculo-venous,  a  compensation  reservoir  for  the  right  ventricle,  2,  584 
None  for  the  left  ventricle,  2 

Elastic  one  to  lessen  the  strain  of  the  ventricular  contraction,  constituted 
by  first  part  of  the  aorta  and  of  the  pulmonary  artery,  74 
Reverberation  as  a  method  of  diagnosis  where  the  stomach  is  concerned,  104,  480 
Reynaud's  disease,  symptoms  of,  due  to  colon  dyspepsia,  (128) 
Rheumatism:  its  influence  on  cardiac  distensibility,  11,  343 
Right  border  of  the  cardiac  dullness  :  its  position  in  anjemic  heart  failure,  239 

Statistics,  354 
Right  Ventricle  (.^ee  also  Ventricle) 

Dilatation  of,  see  Essay  VII,  p.  329;  and  Summary,  pp.  546  to  561 
Adolescent  or  upward  type  of  dilatation,  9 
Its  pathological  aspects,  233,  247,  546 
Its  clinical  aspects,  12,  547 
Its  various  types,  289,  548 
The  usual  one,  289  ;    mainly  upwards,  290 
Mainly  involving  the  conus  arteriosus,  292.  (293),  (294) 
Mainly  outwards  to  the  left,  298 
Adult  type  of  dilatation,  31,  557 

Right  ventricular  overaction  :  its  value  as  a  measure  of  left  ventricular  failure,  47 

Its  diagnostic  value  in  later  life,  86 

Its  absence  in  severe  pneumonia  showing  dangerous  myocardial  weakness, 
(98),  (105) 

Mid-diastolic  murmur,  282 

Third  sound,  282 
'  Rigidity  '  of  the  heart  wall  in  later  life,  definition  of  the  term,  76 

Difficulties  in  diagnosis  due  to  it,  34,  79 

Mechanical  elastic  recoil  due  to  it,  53,  80 

Its  results  in  moderately  strong  hearts,  86 
„       „       in  very  weak  hearts,  91 

Its  clinical  estimation,  147 

A  case  of  weak  heart  showing  its  absence,  (65),  (157) 
Rigidity  of  the  first  part  of  the  aorta,  diagnostic  difficulties  caused  by  it,  74,  109 


SUBJECT   INDEX  G15 

RoUistuii,  Dr.  uu  lu-gaiive  iiitravL-ntiicular  pressure,  412 

Rotation,  after-sensation   following  it,  is  abnormal  in  vertigo  of  non-eardiac 
origin,  121 
Of  the  heart  when  displaced,  37!) 

Sansom,  Dr.,  on  the  third  sound  of  the  heart,  407,  427 

Segmental  pain  in  dilated  deep  thigh-veins,  462 

Semicircular  canals,  hypera.'sthesia  of,  a  useful  sign  in  the  differential  diagnosis 

of  faintness  and  vertigo,  121,  (123) 
Small  heart,  a  sign  of  myocardial  weakness  in  distensible  hearts,  6,  54 
Specific  gravity  of  the  blood  :  its  minimal  level  determinable,  180 
Sphygmomanometer :   dj'spnoea  on  its  application,   a   sign  of  compensatory 

emptiness  of  the  veins,  140 
Sphygmo-oscillomctcr :  its  value  in  determining  the  meaning  of  liigh  blood 

pressures,  144 
Starvation  causing  compensatory  diminution  of  the  blood  volume,  169 
Sternum,  the  percussion  of,  in  relation  to  the  cardiac  dullness,  25 

Sounds  of  the  Heart  : 

Three  sounds  may  mark  the  commencement  of  the  three  phases  of  the 
cardiac  cycle,  399,  428 
Left  ventricular  first  sound  : 

Its  accentuation  a  useful  guide  to  the  increased  ventricuhir  activity  due 

to  raised  blood  pressure,  &c. 
An  absence  of  accentuation  in  spite  of  increased  arterial  resistance  is  a  sign 

of  myocardial  weakness,  146 
Its  accentuation  a  compensatory  phenomenon  in  mitral  stenosis,  390, 4();'5, 418 
Its  feebleness  a  compensatory  phenomenon  in  aortic  regurgitation,  409 

,,  ,,         a  sign  of  myocardial  weakness,  96 

If  sliort  and  sliarp  a  sign  of  lieart  weakness,  96 
Right  ventricular  first  sound  : 

Its  accentuation  a  useful  guide  to  the  anumnt  of  increased  work  done  by 
the  ventricle,  42 
In  failing  compensation  in  valvular  disease,  420 
In  embarrassment  of  the  left  ventricle  in  overstrain,  &c.,  47 
In  anaemia,  244 
Absence  of  accentuation  when  the  pulmonary  circulation  is  embarrassed, 
a  sign  of  myocardial  weakness,  42 
Normal  first  sound  in  severe  pneumonia  a  sign  of  heart  weakness,  (98), { 105) 
Reduplication  of  the  first  sound : 

Spurious  reduplication  can  result  when  in  a  rapid  heart,  a  third  sound 
is  approjcimated  to  the  following  first   sound,  as  with   mid-diastolic 
murmur,  394, 
Second  sound : 

Aortic  accentuated  in  mitral  stenosis  owing  to  increased  ventriculai-  aspira- 
tion, 418,  423 
Pulmonary  second  sound,  550 

Tables  showing  its  loudness  in  valvular  di.sease,  &c.,  421,  423,  424,  &c. 
Its  measured  loudness  in  valvular  disease  when  compensation  is  good 

and  when  imperfect,  423,  424 
Its   apparent    loudness   in   compensated    mitral    stenosis   not    a   true 

accentuation,  392 
Accentuation  in  failing  compensation,  422,  423 
„  ,,    ansemic  heart  failure,  415,  421 

Reduplication  of  the  second  sound,  550 

Pulmonary  half  precedes  the  aortic  in  ananuic  heart  faihire  and  in  left 

ventricular  overstrain,  &c.,  244,  (297) 
Diagnostic  importance  of  aortic  half  preceding  the  pulmonary  half  in 
right  ventricular  failure  secondary  to  high  arterial  rcsi.stance 


016  SUBJECT  INDEX 

Sounds  of  the  Heart  {conlimicd) : 

Third  Sound  of  the  Heart,  282,  340,  395,  407,  427 

Occurs  at  the  commencement  of  t  lie  third  or  relaxation  phase  of  the  heart, 

one-tenth  of  a  second  after  the  second  sound,  399,  428 
Due  to  the  movement  of  the  suddenly  relaxed  segments  of  an  auriculo- 
vcntrieular  valve  if  at  the  moment  of  relaxation  there  be  any  blood 
flowing  through  the  valve  orifice,  396,  431 
In  the  normal  heart  the  flow  has  ceased  prior  to  rela;xation  and  normally 

no  third  sound  occurs,  396,  430 
A  third  sound  gives  evidence  of  prolongation  of  the  flow  from  the  auricle 
into  the  ventricle  :    vide  Mid-diastolic  Murmur,  396,  430 
In  mitral  stenosis,  431 

When  left  auricle  more  dilated  than  left  ventricle,  431 
In  slight  degrees  of  left  ventricular  failure,  431 

right         „  „       in  anaemia,  282,  396,  (441) 

„  ,,  ,,  ,,  ,,       in  overstrain,  (313) 

Cases  showing  character,  &c.,  of  third  sound,  (283),  (284),  &c. 
Possibly  sometimes  due  to  a  preliminary  closing  of  the  auriculo-vcntricular 

valve  at  the  end  of  the  cjcpansion  j)hase,  396 
Effect  of  change  of  posture  on  it,  (284),  (313) 

Suction  recoil  wave  in  the  cardiogram,  407,  (428) 

Suction  by  the  ventricles  (see  Aspiration),  52,  79,  &c. 

'  Superficial '  percussion  dullness,  see  Absolute  Dullness,  21 

Superior  vena  cava  :  its  anatomical  relationship  to  the  fii'st  part  of  the  aorta 

the  cause  of  the  ventricular  wave  in  the  venous  pulse,  512 
„  „  ,,     its    dilatation  the    cause    of    the    superior    vena    cava 

murmur,  44,  218,  561 
Supra-clavicular  fossae,  their  fullness  or  hoUownoss,  of  diagnostic  value  in  heart 

failure,  94,  134,  139 
Syncope,  pallor  in,  450 

Tachycardia  as  a  cardiac  habit,  its  possibility,  325 

Thigh  veins,  dilatation  of,  a  cause  of  nervous  symptoms.  459 

Third  sound  of  the  heart :   vide  Sounds  of  the  Heart,  427 

,,  ,.  its  presence  making  three  diastolic  sounds  audible, 

(284),  (286),  &c. 
„  „  „  its  jiresence    a  means  of  localising  the  interven- 

tricular septum,   284 
Thoracic   viscera  diminish    in  bulk   when  volume  of  l)lood  in  circulation  is 

compensatorily  diminished,  163,  178 
Tonic  muscular  contraction  of  : 
The  right  auricle,  500,  507 

In  relation  to  tricuspid  regurgitation,  38,  503,  509 
The  great  veins,  503,  507 

The  right  ventricle  during  its  relaxation  phase,  505 
Trachea  :    its  lateral  displacement  in  collapse  of  one  lung,  owing  to  a  dia]3lace- 

ment  of  the  mediastinum,  380,  fig.  140 
Tracings  from  the  veins  of  the  neck,  135,  489 
Transverse  contraction  of  muscular  fil)res,  52,  384,  400 

Tricuspid  regurgitation,  phenomena  of,  37.  217.  239,  280,  338  :    vide  Summary, 
p.  559 

Valvular  disease : 
Heart  failure  in,  502 

Early  diagnosis  of  muscular  failure  in,  02,  110 
Estimate  of  rigidity  of  the  heart  wall  in,  150 
Compensation  in,  412 


SUBJECT  INDEX  G17 

Valves  of  veins  of  neck,  their  physiological  functions,  587 

Murmur  due  to  their  incompetence  in  tricuspid  regurgitation,  219,  (291) 
Valves  of  the  heart. 

Theory  of  compensation  in  disease  of  the  mitral  valve,  412 
„  „  „  „  aortic  valves,  347 

Vasomotor  angina,  (127),  (130) 
V^asomotor  disturbance  of  reflex  origin  in  ansumia,  292 

,,  ,,  a  cause  of    intermittent    claudication,   472,   (475), 

(476) 
Veins  of  thigh,  severe  discomfort  due  to  pressure  of  dilated  deep  veins  on  the 

nerve  trunks,  459 
Veins  of  the  neck  : 

False  pulsation  in,  15,  39 

True  pulsation,  16,  39 

Their  emptiness  in  cardiac  embarrassment  a  sign  of  myocardial  weakness, 

61,  (106),  134,  138 
Diagnostic  points  connected  with  them  given  in  tabular  form,  137 
A  visible  diastolic  wave  in  them  is  a  sign  of  rigidity  of  the  right  ventricle, 

398 
Importance  of  noting  their  condition  in  the  heart  failure  of  later  life,  132 
Vena  azygos  in  relation  to  the  auriculo- venous  reservoir,  584,  588,  590,  592 
Venous  pulse  in  the  jugular  bulb,  133 

A  true  measure  of  the  activity  of  the  right  ventricle,  134 
Venous  valves  of  the  subclavian  and  jugular  veins. 

Their  importance  as  a  part  of  the  carcUac  mechanism,  587 
'I'hcir  incompetence  a  cause  of   pulsation  in  the  neck  and  .sometimes  of   a 
murmur,  39,  135,  219,  (291) 
Ventricles  of  the  heart : 

Right  more  easily  studied  than  the  left,  2 

Apportionment  of  strain  between  the  right  and  left  ventricles,  2,  30H,  54  5 
„  „       in  adolescence,  5,  11 

,,  ,,       in  adult  and  later  Ufe,  31 

Diagnostic  importance  of  slight  degrees  of  overaction  of  the  right  as  evidence 

of  the  early  failure  of  the  left,  46 
Dilatation  of,  see  Dilatation 
Theory  of  ventricular  dilatation,  9,  31 

Tonic  activity  of  the  right  ventricle  during  its  relaxation  phase,  510 
Ventricular  expansion,  see  Expansion 

Evidence  of  the  force  developed  by  ventricular  expansion,  436 
Compensatory  dilatation  of   the  left  ventricle  by  its  own  aspiratory  force 

436 
Left  ventricle  sensitive  to  mechanical  stimulation  by  over-distension,  497 
Vertigo  and  faintness  of  labyrinthine  origin  simulating  heart  failure,  121  (123) 
Vertigo  of  non-cardiac  origin  associated  with  hyperajsthcsia  of  the  semicu'cular 
canals,  (123) 

Zinc  and  starcli  dusting  jiuwdcr  a  means  of  writing  upon  the  skin  with  one  of 
tlic  softer  metals,  198 


PEISTED  BT 

SPOTTISWOODE   AND  CO.   LTD.,   COLCH£SIEB 

LONDON   AND  ETON 


Date  Due 

[■^J                              CAT.    NO      ?3    233                             PRINTED    IN    U.S.A. 

Soume.nRe«n^|L.b.aw^^^^^^^^ 


000  522  392     0 


WGliil 
WT53e 
1915 

Wilson,  Theodore  S 

Early  diagnosis  of  heart  failure 


ISSUED    TO 


WGlUl 

WT53e 

1915 
^J'ilson,  Theodore  S 

Earl^  diagnosis  of  heart  failure. 


MEDICAL  SCIENCES  LIBRARY 

UNIVERSITY  OF  CALIFORNIA,  IRVINE 

IRVINE.  CALIFORNIA  92664 


